Thèses : « Central blood pressure levels »

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OCHOA, MUNERA JUAN EUGENIO. « Effects of insulin resistance on systemic haemodynamics and autonomic cardiovascular regulation in normotensive healthy adults ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/46090.

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Hemodynamic effects of insulin resistance (IR) are thought to be largely dependent on its relationship with body mass index (BMI) and blood pressure (BP) levels. The first part of the present thesis was aimed at exploring whether IR is associated with hemodynamic indices of cardiovascular function in a large sample of non-diabetic individuals from the general population (n=731) and if so, to explore if such relationship is continuous across different categories of BMI (lean, overweight and obese), and BP (normal BP, high-normal BP and hypertension). IR was assessed with the homeostasis model assessment of IR (HOMA-IR). Based on a value of HOMA-IR of 2.09 (75th percentile of distribution curve), subjects were classified as insulin-sensitive (IS, HOMA<2.09) or insulin-resistant (IR, HOMA≥2.09). Synchronized beat-to-beat recordings of stroke volume (impedance cardiography) and R-R interval (ECG), along with repeated BP measurements were performed over 5 minutes. Stroke index (SI), cardiac index (CI), systemic vascular resistance index (SVRI), left cardiac work index (LCWI), pre-ejection period (PEP) and left ventricular ejection time (LVET) were computed and averaged. In analysis of co-variance allowing for confounders, IR subjects showed significantly higher BP levels and SVRI, and reduced R-R interval, SI, CI, LCWI, PEP and LVET. These differences remained significant when analyses were performed within each BMI and BP category. Overall, these results indicate that effects of IR on hemodynamic indices of cardiovascular function are continuous across different BMI and BP categories, reinforcing the importance of IR in the pathogenesis of cardiovascular alterations beyond its association with obesity and hypertension. The finding of a significant association between IR and hemodynamic alterations even in lean and normotensive subjects was the rationale to explore potential mechanisms for these alterations in this selected group of subjects. Specific objectives of this second part of the thesis were: 1) To explore the relationship between insulin resistance and systemic hemodynamics, cardiac baroreflex sensitivity and indices of autonomic CV modulation. 2) To explore the relationship of insulin resistance with 24h heart rate, average blood pressure levels and blood pressure variability over the 24h; and 3) To explore the relationship of insulin resistance with central blood pressure levels and with measures of large artery stiffness and wave reflections. The study population for these analyses was constituted by subjects who were below the 30th percentile of diastolic blood pressure (DBP) distribution curve (DBP ≤72 mmHg) and who had no elevation in systolic BP levels. In addition, subjects were excluded in case of diabetes mellitus (fasting blood glucose ≥126 mg/dL or use of medications for previously diagnosed type 2 diabetes) obesity (BMI≥30) or taking medications with effects on BP. A total of 90 subjects fulfilling inclusion criteria were considered for the present analysis and underwent further assessments. Insulin resistance was assessed with HOMA-index and subjects classified into IR tertiles, based on the distribution of HOMA-index values. 24h Ambulatory BP monitoring was performed. Mean SBP and DBP were averaged for the day, night and 24h, and the respective day-to-night dipping was calculated. BPV was assessed for SBP and DBP as 24h standard deviation (SD), weighted 24h SD (wSD), daytime and night-time SD. Recordings of pulse waveform were obtained by means of a previously validated oscillometric device for ambulatory BP monitoring with in-built transfer-function like method. Aortic pulse wave velocity (PWV, m/s) and other measures derived from pulse wave analysis such as augmentation index (AIx, %), central SBP (cSBP), central DBP (cDBP) and central pulse pressure (cPP) were computed. Peripheral SBP and DBP, and heart rate (HR) were recorded and pulse pressure (PP) calculated as the difference between SBP and DBP. Non-invasive assessment of beat-to-beat BP, R-R interval (ECG) and stroke volume (by means of impedance cardiography) were performed during 10 min in supine position and specific hemodynamic indices associated with their measurement were computed and averaged: RRI (msec), heart rate (HR, bpm), stroke volume index (SI, mL/beat/m2), cardiac index (CI, L/min/m2), SBP (mmHg) and DBP (mmHg), systemic vascular resistance index (SVRI, dyn/sec/cm-5/m2), left cardiac work index (LCWI, Kg/m/m2), pre-ejection period (PEP, msec), left ventricular ejection time (LVET, msec) and PEP/LVET ratio were calculated. Cardiac autonomic modulation was assessed by computer analysis of 10 min beat-to-beat BP and ECG recordings in resting supine position. Cardiac baroreflex sensitivity (BRS) was estimated by sequence method. Total variance, low-frequency (LF) and high-frequency (HF) spectral components of HR variability (HRV) were assessed by autoregressive analysis. LF/HF ratio was calculated. After multiple regression analysis, adjusting for common confounders such as age, sex, HR and BMI, increasing values of HOMA-IR were associated with reduced RRI, SI, CI, and with increased SVRI, SBP and DBP. IR was also associated with reduced BRS (up, down, and total slopes), decreased parasympathetic indices of autonomic CV modulation (SDRRI, HF-power, total power) and a predominance of sympathetic component of HRV (increased LF/HF ratio). Increasing values of HOMA-IR were also associated with increased HR and average SBP levels (during day, night and 24-h period), with augmented BP variability (Day SBP SD, and SBP wSD) and with a reduced dipping of HR. Finally, insulin resistance was shown to be associated with increasing values of aortic PWV, and with higher central and peripheral SBP and DBP levels. Overall, these results support significant associations between insulin resistance and changes in hemodynamic and autonomic indices of cardiovascular function, even after accounting for common confounders. These findings suggest that in normotensive healthy adults, increases in insulin resistance may promote alterations in autonomic cardiovascular modulation, in systemic hemodynamics and in arterial stiffness, all of which are known contributors to the pathogenesis of hypertension.

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Guilcher, Antoine. « Central blood pressure ». Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/central-blood-pressure(cfe1a0fc-56e8-4338-a6aa-462c6d6de0bb).html.

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Central aortic systolic blood pressure (cSBP) differs from peripheral systolic blood pressure (pSBP) measured in the arm. cSBP may be estimated non-invasively by application of a generalised transfer function (GIF) to a high fidelity peripheral arterial waveform or from the late systolic shoulder (SBP2) of such a waveform. The relative accuracy of these estimates and the degree to which they depend on the accuracy of peripheral blood pressure is unknown. The interest in estimates of central blood pressure is driven in large part by the fact that aortic pulse pressure (cPP) is thought to be a better predictor of cardiovascular risk and response to antihypertensive treatment than peripheral BP. However, little is known concerning the mechanism by which drugs may reduce cPP independently of effects on peripheral BP. Objectives of this thesis were to: 1. Examine the relative accuracy of different methods (GTF and SBP2) for estimating cSBP and cPP from a high fidelity peripheral arterial waveform. 2. Determine errors introduced by non-invasive calibration of this waveform (as would be the case when such methods are used in practice), 3. Explore the use of a simplified method for estimating cSBP based upon pressure oscillations within an arm cuff. 4. Determine the mechanism by which nitroglycerin (NTG, a drug that has relatively selective actions to lower cSBP) lowers cPP. Pressure and in some cases combined pressure and flow velocity were acquired at the aortic root during cardiac catheterisation. Peripheral blood pressure was measured by oscillometry and peripheral blood pressure waveforms were obtained from blood pressure cuffs, radial tonometry and a servo-controlled finger cuff. To address objective 4 additional measurements of ventricular and arterial mechanics where made using ultrasound and magnetic resonance imaging.

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Brunström, Mattias. « Effect of antihypertensive treatment at different blood pressure levels ». Doctoral thesis, Umeå universitet, Medicin, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-143061.

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Background High blood pressure is associated with an increased risk of cardiovascular disease and premature death. The shape of association between blood pressure and the risk of cardiovascular events is debated. Some researchers suggest that the association is linear or log-linear, whereas others suggest it is J-shaped. Randomized controlled trials of antihypertensive treatment have been successful in hypertension, but ambiguous in the high normal blood pressure range. Previous systematic reviews have not found any interaction between baseline systolic blood pressure and treatment effect, with beneficial effects at systolic blood pressure levels well below what is currently recommended. These reviews, however, use a method to standardize treatment effects and study weights according to within-trial blood pressure differences that may introduce bias. Methods We performed two systematic reviews to assess the effect of antihypertensive treatment on cardiovascular disease and mortality at different blood pressure levels. The first review was limited to people with diabetes mellitus. The second review included all patient categories except those with heart failure and acute myocardial infarction. Both reviews were designed with guidance from Cochrane Collaborations Handbook for Systematic Reviews of Interventions, and are reported according to PRISMA guidelines. We included randomized controlled trials assessing any antihypertensive agent against placebo or any blood pressure targets against each other. Results were combined in random-effects meta-analyses, stratified by baseline systolic blood pressure. Non-stratified analyses were performed for coronary heart disease trials and post-stroke trials. Interaction between blood pressure level and treatment effect was assessed with Cochran’s Q in the first review, and multivariable-adjusted metaregression in the second review. The third paper builds on data from the second paper, and assesses the effect of standardization according to within-trial blood pressure differences on the results of meta-analyses. We performed non-standardized analyses, analyses with standardized treatment effects, and analyses with standardized treatment effects and standard errors. We compared treatment effect measures and heterogeneity across different methods of standardization. We also compared treatment effect estimates between fixed-effects and random-effects meta-analyses within each method of standardization. Lastly, we assessed the association between number of events and study weights, using linear regression. Results Forty-nine trials assessed the effect of antihypertensive treatment in people with diabetes mellitus. Treatment effect on cardiovascular mortality and myocardial infarction decreased with lower baseline systolic blood pressure. Treatment reduced the risk of death and cardiovascular disease if baseline systolic blood pressure was 140 mm Hg or higher. If baseline systolic blood pressure was below 140 mm Hg, however, treatment increased the risk of cardiovascular death by 15 % (0-32 %). Fifty-one trials assessed the effect of antihypertensive treatment in primary prevention. Treatment effect on cardiovascular mortality, major cardiovascular events, and heart failure decreased with lower baseline systolic blood pressure. If baseline systolic blood pressure was 160 mm Hg or higher treatment reduced the risk of major cardiovascular events by 22 % (95 % confidence interval 13-30 %). If systolic blood pressure was 140-159 mm Hg treatment reduced the risk by 12 % (4-20 %), whereas if systolic blood pressure was below 140 mm Hg, treatment effect was neutral (4 % increase to 10 % reduction). All-cause mortality was reduced if systolic blood pressure was 140 mm Hg or higher, with neutral effect at lower levels. Twelve trials compared antihypertensive treatment against placebo in people with coronary heart disease. Mean baseline systolic blood pressure was 138 mm Hg. Treatment reduced the risk of major cardiovascular events by 10 % (3-16 %), whereas the effect on mortality was neutral (7 % increase to 11 % reduction). Standardization of treatment effects resulted in more extreme effect estimates for individual trials. This caused increased between-study heterogeneity, and different results with fixed- and random-effects model. Standardization of standard errors shifted weights from trials with many events to trials with large blood pressure differences. This caused biased overall effect estimates. Standardization of standard errors also resulted in wider confidence intervals, masking the previously increased heterogeneity. This reduced the possibility to find different treatment effects at different blood pressure levels. Conclusion The effect of antihypertensive treatment depends on blood pressure level before treatment. Treatment reduces the risk of death and cardiovascular disease if baseline systolic blood pressure is 140 mm Hg or higher. Below this level, treatment is potentially harmful in people with diabetes, has neutral effect in primary prevention, but might offer additional protection in people with coronary heart disease. Standardization should generally be avoided in meta-analyses of antihypertensive treatment. Previous meta-analyses using standardized methods should be interpreted with caution.
Hjärt-kärlsjukdomar leder till fler dödsfall och fler förlorade levnadsår än någon annan sjukdomsgrupp. Den enskilt viktigaste riskfaktorn som bidrar till hjärtkärlsjukdomar ur ett befolkningsperspektiv är högt blodtryck. Risken att drabbas av hjärt-kärlsjukdomar minskar om man behandlar högt blodtryck men till vilken nivå blodtrycket skall behandlas är kontroversiellt. Denna avhandling innefattar två systematiska översikter och meta-analyser samt ett arbete som jämför olika sätt att hantera skillnader mellan studier i meta-analyser. De systematiska översikterna sammanställer data från randomiserade kontrollerade studier av blodtryckssänkande behandling. Vår övergripande frågeställning var om effekten av behandling påverkas av blodtrycksnivån innan behandling. Mer specifikt studerades hur behandling påverkade risken att dö eller drabbas av hjärt-kärlsjukdom vid olika blodtrycksnivåer. Det första arbetet fokuserade på personer med diabetes. För dessa fann vi att blodtryckssänkande behandling minskar risken att dö eller drabbas av hjärtkärlsjukdom vid nivåer ≥ 140 mmHg. Vi fann ingen nytta, men möjligen en skadlig effekt av behandling, vid lägre blodtrycksnivåer. Det andra arbetet inkluderade studier oberoende av vilka sjukdomar deltagarna hade. Vi fann att den förebyggande effekten av blodtryckssänkande behandling berodde på blodtrycksnivån. Vid blodtryck > 160 mmHg minskade risken att drabbas av hjärt-kärlsjukdomar med 22 % hos de som erhöll behandling. Om blodtrycket var 140-160 mmHg minskade risken med 12 %, men om blodtrycket var < 140 mmHg sågs ingen behandlingseffekt. Hos personer med känd kranskärlssjukdom, och ett medelblodtryck på 138 mmHg, fann vi en något minskad risk för hjärt-kärlhändelser med ytterligare behandling. I det tredje arbetet fann vi att skillnader i resultat mellan olika studier inte kan antas bero endast på olika grad av blodtryckssänkning i studierna. När resultaten standardiserades, som om alla studier hade sänkt blodtrycket lika mycket, ökade nämligen skillnaderna mellan studierna. Detta resulterade i sin tur i snedvridning av resultaten från meta-analyser av standardiserade värden. Sammanfattningsvis minskar blodtryckssänkande behandling risken att dö eller drabbas av hjärt-kärlsjukdomar om blodtrycket är 140 mmHg eller högre. Vid lägre nivåer är nyttan med behandling osäker samtidigt som det finns potentiella risker. Standardisering bör inte användas rutinmässigt vid metaanalyser av blodtrycksstudier. Tidigare meta-analyser som använt denna metod bör tolkas med försiktighet.

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Lanor, Frank. « Predictors of Blood Pressure and Lipids Levels Among African Americans ». ScholarWorks, 2018. https://scholarworks.waldenu.edu/dissertations/5742.

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African Americans disproportionately develop cardiovascular disease risk factors including high blood pressure and high cholesterol levels in comparison to European Americans. The purpose of this study was to examine the associations of diet quality and physical activity with blood pressure levels and cholesterol levels among African Americans. The social ecological model was the theoretical foundation for the study. Research questions were designed to examine the extent to which diet quality and physical activity predict blood pressure levels and cholesterol levels. The research design was quantitative cross-sectional secondary analysis of 959 participants. After controlling for demographic factors, body mass index, and energy intake, there was a potential nonlinear association between the dietary approaches to stop hypertension (DASH) diet and blood pressure levels. Multivariable-adjusted logistic regression analysis showed that a fourth-quintile DASH score significantly predicted blood pressure (OR: 0.57; 95% CI [0.35, 0.93]). There was no association between the DASH diet and cholesterol levels. Physical activity was not significantly associated with blood pressure levels or cholesterol levels. Researchers can use these findings to replicate large prospective studies. In addition, findings may be used to promote positive social change by healthcare professionals including dieticians and clinicains, as well as health promotion advocates and other institutions or individuals with public health interest.

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Kumagai, Kyoko. « Central blood pressure relates more strongly to retinal arteriolar narrowing than brachial blood pressure : The Nagahama Study ». Kyoto University, 2015. http://hdl.handle.net/2433/199173.

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Wijkman, Magnus. « Acute, ambulatory and central blood pressure measurements in diabetes ». Doctoral thesis, Linköpings universitet, Internmedicin, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-75352.

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Background: In patients with diabetes, high blood pressure is an established risk factor for cardiovascular disease. The aim of this thesis was to explore the associations between blood pressure levels measured with different techniques and during different circumstances, and the degree of cardiovascular organ damage and subsequent prognosis in patients with diabetes. Methods: We analysed baseline data from patients with type 2 diabetes who participated in the observational cohort study CARDIPP (Cardiovascular Risk factors in Patients with Diabetes – a Prospective study in Primary care), and longitudinal data from patients registered in the Swedish national quality registry RIKS-HIA (Register of Information and Knowledge about Swedish Heart Intensive care Admissions). Patients in CARDIPP underwent nurse-recorded, 24-hour ambulatory and non-invasive central blood pressure measurements. Patients in RIKS-HIA had their systolic blood pressure measured upon hospitalisation for acute chest pain. Results: In CARDIPP, nearly one in three patients with office normotension (<130/80 mmHg) were hypertensive during the night (≥120/70 mmHg). This phenomenon, masked nocturnal hypertension, was significantly associated with increased arterial stiffness and increased central blood pressure. Furthermore, nearly one in five CARDIPP patients with office normotension had high central pulse pressure (≥50 mmHg), and there was a significant association between high central pulse pressure and increased carotid intima-media thickness and increased arterial stiffness. Among CARDIPP patients who used at least one antihypertensive drug, those who used beta blockers had significantly higher central pulse pressure than those who used other antihypertensive drugs, but there were no significant between-group differences concerning office or ambulatory pulse pressures. In CARDIPP patients with or without antihypertensive treatment, ambulatory systolic blood pressure levels were significantly associated with left ventricular mass, independently of central systolic blood pressure levels. When RIKS-HIA patients, admitted to hospital for chest pain, were stratified in quartiles according to admission systolic blood pressure levels, the risk for all-cause one-year mortality was significantly lower in patients with admission systolic blood pressure in the highest quartile (≥163 mmHg) than in patients with admission systolic blood pressure in the reference quartile (128-144 mmHg). This finding remained unaltered when the analysis was restricted to include only patients with previously known diabetes. Conclusions: In patients with type 2 diabetes, ambulatory or central blood pressure measurements identified patients with residual risk factors despite excellent office blood pressure control or despite ongoing antihypertensive treatment. Ambulatory systolic blood pressure predicted left ventricular mass independently of central systolic blood pressure. In patients with previously known diabetes who were hospitalised for acute chest pain, there was an inverse relationship between systolic blood pressure measured at admission and the risk for one-year all-cause mortality.

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Smith, Wendy. « Lifetime stress, blood pressure, heart rate, and salivary cortisol levels in post-menopausal women ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ40186.pdf.

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Paul, Erin E. « Central hemodynamic responses to an acute sodium load ». Access to citation, abstract and download form provided by ProQuest Information and Learning Company ; downloadable PDF file 0.33 Mb., 63p, 2005. http://wwwlib.umi.com/dissertations/fullcit/1428183.

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Camacho, Fernando Graduate School of Biomedical Engineering Faculty of Engineering UNSW. « Statistical analysis of central aortic blood pressure parameters derived from the peripheral pulse ». Awarded by:University of New South Wales. Graduate School of Biomedical Engineering, 2006. http://handle.unsw.edu.au/1959.4/26215.

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With the rise in prevalence of cardiovascular (CV) disease, risk stratification is becoming increasingly important. Accurate characterization of the CV system is required, for which central aortic blood pressure (BP) parameters form an integral part. However, invasive measurement of central aortic BP parameters (aP) is difficult. Therefore, non-invasive methods to estimate aP from the radial pressure pulse (rPulse) have been proposed. To analyze accuracy of estimated aP (aPhat) and applicability in risk stratification and diagnosis, this study presents: (1) a novel representation of the rPulse with minimal loss of information, (2) a framework for strict definition and statistical analysis of aPhat, and (3) a dynamic analysis of effects of mean BP (MP) and heart rate (HR) in the rPulse shape. Methods: (1) 2671 rPulse s measured by applanation tonometry were represented using the first eight principal components (PC) scores after standard PC transformation. rPulse shapes were compared in three subpopulations. (2) The concept of "estimation option" (EO) for aP estimation was presented. A framework for strict definition of aPhat and the comparison of EOs was proposed, and 7 different EOs compared. (3) A sequence of rPulse s was analyzed during soft exhalation maneuver (SEM) %, a mild Valsalva type maneuver, in eight healthy subjects. Radial BP and respiration pressure were continuously measured. The effects of MP and HR in the rPulse parameters were analyzed by standard linear regression for each subject. Results: (1) PC representation of the rPulse improves accuracy of the estimation of aPhat compared with the simple use of rPulse parameters. Subpopulations have distinctive rPulse shapes. (2) No single EO was better for the estimation of all aPhat. Inclusion of MP improves estimation accuracy. Despite further improvement when rPulse is included, the general transfer function EO is a biased estimator. (3) The dynamic analysis of the rPulse provides information of the effects of MP and HR in the rPulse not available in static analysis. The effects were specific for each individual and different from the results obtained from a general population. Conclusions: For accurate CV risk stratification, future studies should include a dynamic measurement of calibrated radial pressure pulse during SEM maneuver. Risk analysis and diagnosis should be based on representations of the rPulse with minimum loss of information. aPhat should be used for better understanding of the underlying physiological principles.

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Elliott, Joseph Rothora. « The applicability of the Theory of Planned Behaviour in the management of blood pressure levels ». Thesis, University of East London, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306425.

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Knowles, Ian David. « The role of 5-HTâ†2 receptors in central cardiovascular regulation in anaesthetized rats ». Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313783.

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Cai, Ye Tan. « Assessment of central arterial hemodynamics, arterial stiffness, and vascular structure in children and adolescents ». Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/22921.

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Background Central arterial hemodynamics, arterial stiffness and arterial structure are predictive of cardiovascular events and outcomes in adulthood. The tools to measure these parameters have largely been developed and validated in adults, but poorly investigated in children. With increasing interest in cardiovascular risk assessments earlier in life, it is imperative to critically appraise the techniques to measure these parameters in childhood to ensure validity of measurement, and to understand what these parameters mean with regards to association with future cardiovascular disease outcomes. Aims We sought to test whether the currently available methodologies for assessing central arterial hemodynamics and arterial stiffness in adults would be similarly accurate and valid in children. These included the use of generalized transfer functions to estimate central hemodynamic parameters, and methods for estimating pulse wave velocity. Furthermore, we aimed to explore carotid extra-medial thickness as a potential cardiovascular risk marker in childhood. This included determining the association between carotid extra-medial thickness, a measure of arterial adventitial structure, and arterial stiffness in early life. Results In chapter 2, 3, 4, and 5 we found that adult transfer functions are sufficient for central blood pressure assessment in early life with correct pulse pressure calibration, but age-appropriate transfer functions are required for more accurate assessment of central waveform features in children. In chapter 6, we find that pulse wave velocity can be accurately measured in children and adolescents using a leg cuff-based approach, but can be improved upon with age-appropriate algorithm changes. In chapter 7 and 8, we found a small but significant association between carotid extra-medial thickness and carotid artery stiffness in children, but no association between this measure of arterial structure and cardiovascular outcomes later in life. Conclusions Assessments of central arterial hemodynamics and arterial stiffness in children benefit from age-appropriate adjustments to their measurement methodologies. Carotid adventitial structure, while associated with arterial stiffness in early life, is not a predictor of cardiovascular outcomes in adulthood.

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Puglisi, Janis Panzenhagen. « The association of vitamin D levels, blood pressure, inflammation and depression in persons with coronary artery disease ». Thesis, The University of North Carolina at Greensboro, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3624222.

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The purpose of this study was to examine the association of demographic factors, serum Vitamin D levels, hypertension (HTN) (by HTN diagnosis, systolic blood pressure [SBP] and diastolic blood pressure [DBP]), serum (hs-CRP) and endothelial measures of inflammation upon the prevalence of depression in adults with coronary artery disease (CAD) from central North Carolina. A literature derived theory, the Puglisi Model of Vitamin D Levels' Associations with Depression, guided this study. Vitamin D levels, measures of blood pressure, and serum and endothelial measures of inflammation, were theorized as being associated with depression.

A cross-sectional, associational design was employed in the parent study from which previously frozen alliquoted blood of subjects with CAD was further analyzed to assess the serum Vitamin D levels and liver function. This convenience sample of 101 persons with CAD who presented between 2007 and 2010 at the University of North Carolina Hospital's Cardiac Catheterization lab was utilized. The majority of the sample of well-controlled persons with CAD was male (66%), White (81%), had hypertension (81%), and low serum Vitamin D levels (82%). Depression, found as a diagnosis in 27%, was not significantly associated with Vitamin D levels (p = 0.17), even when controlling for demographic factors (AOR 0.96; p = 0.13; 95% CI [.90 - 1.01]). There were no differences between brachial artery flow mediated dilation (BAFMD), augmentation index, and high sensitivity C-reactive protein (hs-CRP) by depression group, but there was for reactive hyperemia index (RHI) [t = 1.97; df = 99; p = 0.05]. Vitamin D levels were inversely associated with both SBP (p < 0.001) and DBP (p < 0.001), but Vitamin D levels were not associated with a diagnosis of HTN (AOR 0.97; p = 0.28; 95% CI [.92, 1.02]. Controlling for the potential confounders of age, sex, race, body mass index, liver and kidney functions did not alter the significant association between Vitamin D levels and SBP and DBP (p = 0.05). Vitamin D levels were significantly associated with two inflammatory measures—hs-CRP and augmentation index, but not with BAFMD and RHI. When controlling for age, sex, race, BMI and Vitamin D levels, only hs-CRP but none of the three endothelial measures of inflammation (RHI, BAFMD nor augmentation index [AI]), were associated with depression (AOR 0.956; p = 0.13; 95% CI [.90, 1.01]).

Nurses should be aware that most of the adults with CAD herein had low or insufficient Vitamin D levels, and that Vitamin D levels may significantly affect SBP and DBP in persons with CAD and perhaps other populations as well. Many persons have depression around the time of their cardiac event or thereafter. Because increased morbidity and mortality occur in individuals with decreased Vitamin D levels, and depression, even when identified and treated in persons with CAD is associated with worsened outcomes, appropriate screening for and treatment of low serum Vitamin D levels is needed. Thus, advanced practice clinicians caring for persons with CAD should encourage screening of Vitamin D levels, and treatment of low levels with appropriate supplementation.

Further studies are needed to explore why some endothelial measures are associated with Vitamin D levels and depression, and others are not. Additional studies should seek to confirm the inverse association of Vitamin D levels with SBP and DBP while accounting for season of the year and other potential confounders. Finally, studies should utilize a depression screening tool to test the Puglisi model's proposed association between low Vitamin D levels with an increased occurrence of depression in both persons with CAD and other populations.

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Wiley, Kyle Steven. « Linking Self-Perception of Stressful Experiences with Blood Pressure and Salivary Cortisol Levels in Undergraduate College Students ». Thesis, The University of Arizona, 2013. http://hdl.handle.net/10150/297793.

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A large body of research suggests self-perception of stressful experiences is not always a good predictor of stress biomarkers. On this front, anthropologists have an opportunity to disentangle the interactions between individual perceptions of stress and the stress response. To better understand these interactions we chose a sampling frame that allows individual participants to self-identify as high, medium, and low stress responders. We chose to conduct this research in an undergraduate student community for two reasons: 1) final exams serve as a similarly timed stressor, 2) given the perceived stress associated with student work loads, recruitment should be easier in an undergraduate community. With two data collection points, we recruited and sampled thirty-two students. Stress biomarker data include blood pressure and salivary cortisol, analyzed using Salimetrics high sensitivity salivary cortisol enzyme immunoassay kits. A short questionnaire was used to indicate an individuals’ perception of the role of stress in their lives. Our interview data suggest an awareness of highly variable responses to stress. By comparing the interview data to stress biomarkers across self-designated categories of stress reactions we plan to link variation in perception, reactivity, and biomarkers to develop a more nuanced understanding of the stress response and its physiological outcomes.

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Leibold, Nancyruth Hawkins Peggy L. Morin Patricia J. McKinney-Williams Angela. « The effect of a school nurse led education intervention on blood pressure and physical activity levels in adolescents ». Click here for access, 2009. http://www.csm.edu/Academics/Library/Institutional_Repository.

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Thesis (Ed. D)--College of Saint Mary -- Omaha, 2009.
A dissertation submitted by Nancyruth Leibold to College of Saint Mary in partial fulfillment of the requirement for the degree of Doctor in Education with an emphasis on Health Professions Education. This disseratation has been accepted for the faculty of College of Saint Mary by: Peggy Hawkins, RN, PhD, chair ; Patricia J. Morin, RN, PhD, committee member ; Angela McKinney-Williams, PhD, committee member. Includes bibliographical references.

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Serinel, Yasmina. « Novel Methods for Treating and Assessing Hypertension in Obstructive Sleep Apnoea ». Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20445.

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In this thesis, the primary motivation was to develop a strategy to help improve the treatment of hypertension in patients with obstructive sleep apnoea (OSA), and to discover new biomarkers of risk that can be used for future prognostication and for therapeutic interventions. A central theme throughout is the emphasis on analysing and targeting the 24 hour blood pressure profile of patients with OSA, given our newer understanding that nocturnal blood pressure is the strongest predictor of cardiovascular mortality. Chapter 1 is a comprehensive literature review covering blood pressure physiology, the pathophysiology of hypertension and arterial stiffness both in non-OSA and OSA populations and treatment strategies including chronotherapy. In chapter 2 we explore the use of chronotherapy, or the altered timing of once-daily medication administration, in a randomised double blinded placebo controlled trial, in an effort to improve the blood pressure control of patients with OSA. In chapter 3, we explored 24 hour arterial haemodynamics in patients with OSA as a novel biomarker for future risk stratification and therapeutic interventions with the use of state-of-the-art technology. In the final chapter we summarise the key findings of our studies and briefly discuss future directions.

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Kiru, Gayithri. « Investigating the roles of peripheral and central blood pressure and blood pressure variability on the size and growth rate of AAAs in the AARDVARK trial and the CAVE sub-study ». Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/53377.

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The AARDVARK (Aortic Aneurysmal Regression of Dilation: Value of ACE-Inhibition on RisK) trial was designed to investigate whether ACE-inhibition reduces the growth rate of small abdominal aortic aneurysms (AAA), independent of blood pressure (BP) lowering. A cohort of patients from the AARDVARK trial contributed data to the CAVE sub-study which investigated the roles of peripheral and central BP and 3 measures (standard deviation, coefficient of variation and variation independent of the mean) of visit-to-visit BP variability (BPV) of peripheral and central BPs on the size and growth rate of the diameters of small AAAs. Subjects aged ≥55 years with AAA diameter 3.0–5.4 cm were randomised 1:1:1 to receive perindopril 10 mg, or amlodipine 5 mg, or placebo. Three standardised BP measurements and an AAA ultrasound scan were performed at every trial visit (every 3-6 months over 2 years). Five of 14 trial sites were provided with a BP+ machine which measures both peripheral and central BP. Nine sites collected peripheral BP only with an Omron machine. BPV was based on readings taken after 3 months to avoid confounding from the impact of trial treatments. The primary outcome of the AARDVARK trial was AAA diameter growth (based on external antero-posterior ultrasound measurements in the longitudinal plane), determined by multi-level modelling. 224 patients were randomised between 2011 and 2013 to receive either placebo (n = 79), perindopril (n = 73), or amlodipine (n = 72). Mean baseline age, peripheral BP and AAA size among the 224 patients who contributed peripheral BP data were 71.3 years, 131.5/77.7 mmHg and 4.0cm (external diameter) respectively and were not significantly different from the 139 patients who also contributed central BP data. No significant differences in the modelled annual growth rates were apparent among the 3 randomised groups [placebo 1.68 mm (SE 0.2), perinodopril 1.77 mm (0.2), and amlodipine 1.81 mm (0.2), respectively]. The estimated difference in annual growth between the perindopril and placebo group was 0.08 mm (CI 20.50, 0.65). No evidence of an association was found between peripheral or central BP and AAA size at baseline or AAA growth in-trial. However, significant associations were found between central (but not peripheral) BPV and AAA growth using linear regression after adjustment for possible confounders. This association was stronger for central diastolic than systolic BPV. Evidence of a dose-response effect (albeit underpowered due to this comparison being restricted to quartiles) was apparent, with patients having the most variable central BP exhibiting the highest AAA growth rates. In the AARDVARK trial, small AAA growth rates were lower than anticipated thereby reducing the power of the trial, but there was no apparent impact of perindopril compared with placebo or placebo and amlodipine combined on AAA growth rates, despite more effective BP lowering among those allocated to perindopril. However by contrast, in the CAVE sub-study we showed a significant association between all 3 measures of central BPV and AAA growth despite the small sample size and limited numbers of visits. A larger study is required to confirm these results.

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Kumasawa, Junji. « Detecting central-venous oxygen desaturation without a central-venous catheter : utility of the difference between invasively and non-invasively measured blood pressure ». 京都大学 (Kyoto University), 2016. http://hdl.handle.net/2433/217144.

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Pollard, Tessa M. « Variation in mood, adrenal 'stress' hormone levels with blood pressure associated with everyday working experience in a British population ». Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386582.

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Sheu, Bryan. « Levels of neutrophils stimulation and matrix Metalloprotease in plasma of individuals with elevated blood pressure and acute / long-term exercise ». Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p1453018.

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Thesis (M.S.)--University of California, San Diego, 2008.
Title from first page of PDF file (viewed June 25, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 60-65).

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Rosa, Alexandre Antonio Marques. « "Monitorização ambulatorial da pressão arterial de pacientes com oclusão do ramo da veia central da retina" ». Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5149/tde-26012006-163810/.

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Avaliou-se a prevalência de hipertensão arterial sistêmica (HAS) e a variação circadiana da pressão arterial (PA), através da Monitorização ambulatorial da pressão arterial (MAPA), em pacientes com oclusão do ramo da veia central da retina (ORVCR). Foram avaliados, prospectivamente, 93 casos/olhos de 83 pacientes. A ausência do descenso fisiológico da PA durante o sono ("non-dipper") foi definida como diminuição da pressão sistólica = 10% e a presença de descenso quando este valor fosse maior ("dipper"). Há uma prevalência extremamente alta (94%) de HAS em pacientes com ORVCR. Entre os hipertensos, uma grande parcela dos indivíduos "non-dipper" (n=34; 44,2%). Estas evidências sugerem que um nível mais sustentado de PA nas 24 horas possa ser um fator de risco para o desenvolvimento da ORVCR
Objective: Identifying with Blood pressure monitoring (BPM) in patients with branch retinal vein occlusion (BRVO): high blood pressure (HBP) prevalence, possible cases of white-coat normotension (WCNT) and variation of circadian blood pressure (BP). Methods: Prospectively, 93 cases/eyes of 83 patients with BRVO were evaluated at Ophthalmological Clinic of "Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo" (HCFMUSP). After that, patients were taken to Hypertension League of Nephrology Chair of HCFMUSP (LH-HCFMUSP) for clinical evaluation and blood pressure monitoring. Non-dipper was defined as a fall in systolic blood pressure = 10%, and dipper when this value was higher

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Nelson, William Bradley. « Exercise Induced Hypervolemia : Role of Exercise Mode ». Diss., CLICK HERE for online access, 2007. http://contentdm.lib.byu.edu/ETD/image/etd2128.pdf.

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McNairn, Julie Anne. « The central regulation of blood pressure and salt appetite by brain 11β- hydroxysteroid dehydrogenase type 2 : a novel gene targeting technique ». Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31048.

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Hypertension is the chronic elevation in blood pressure that is regulated in part through the retention and regulation of sodium retention and excretion in the kidneys. Hence the kidney has been considered the organ that regulates blood pressure. There are a cohort of patients that suffer with high blood pressure due to lack of 11β-hydroxysteroid dehydrogenase-type 2 (11β-HSD2) expression (which inactivates glucocorticoids (GCs), allowing selective activation of mineralocorticoid receptors (MR) by aldosterone) that results in hypertensive and increased salt appetite phenotypes - a condition known as syndrome of apparent mineralocorticoid excess (SAME). This disorder can be recapitulated in the mouse through the global deletion of 11β-HSD2, which results in over activation of the MR driving an elevation in blood pressure. However, the distinction between blood pressure elevation because of kidney dysfunction with loss of 11β-HSD2 or increased salt appetite due to loss of brain 11β-HSD2 expression is not clear from the global 11β-HSD2 knockout model. Salt appetite is regulated by regions of the brain out-with the blood-brain barrier, known as circumventricular organs. In the mouse, salt appetite is controlled by aldosterone-sensitive cells in the nucleus of the solitary tract (NTS) in the brain stem, where 11β-HSD2 is expressed to provide mineralocorticoid selectivity. However, in the fetal brain, 11β-HSD2 is widely expressed, protecting against adverse GC action that alters brain development and increases susceptibility to psychiatric disorders as adults. 11β-HSD2 deletion solely in the brain from embryonic day 12 resulting in GC fetal programming (HSD2BKO) causes effects on both behaviour and salt appetite. To determine the role of developmental versus adult expression of brain 11β- HSD2, mice with deletion of brain 11β-HSD2 from mid gestation (HSD2BKO) and mice with adult deletion of 11β-HSD2 in the NTS using lentivirus (HSD2.v- BKD) were compared. The phenotypes (salt appetite, blood pressure (BP), baroreceptor response (BRR) and cognition), can be categorised as either due to GC fetal programming (as indicated by HSD2BKO groups), or increased activation of MR in adult 11β-HSD2 expressing neurons (recapitulated in the HSD2.v-Cre groups). Salt appetite increased in both HSD2BKO and HSD2.v-BKD cohorts (mean percentage increase 65% n=8 and 46% n=6, compared to their respective controls), leading to an increased BP in both groups (+12% and +8%, respectively) as well as an impaired BRR, indicating all phenotypes are mediated by adult NTS neurons. However, spatial recognition memory (Object-in-Place task) is abolished in HSD2BKO mice, whereas, HSD2.v-BKD mice still retain short-term memory. Our data suggest that neural 11β-HSD2 protects against inappropriate activation of MR by corticosterone to regulate salt appetite and salt-induced rises in blood pressure. However, spatial recognition memory is not influenced by deletion of 11β-HSD2 in the adult brain, confirmation that this phenotype is underpinned by developmental programming by GCs, which is observed in the 11β-HSD2 brain KO. Salt appetite has been shown to be centrally regulated through the adult deletion of 11β-HSD2. From this, our data suggest that an increased salt appetite is due to adult loss of function of 11β-HSD2 rather than GC programming during development. Highlighting the NTS as a region for drug delivery to try and control salt appetite in salt sensitive individuals who struggle with administering a recommended change in diet. To develop this further, minimally invasive modes of delivery of viruses and drugs into the brain were investigated. In so doing, a non-invasive and reversible method to temporarily disrupt the blood brain barrier (BBB) was optimised. The technique required acoustic insonation of ultrasonic contrast agents (CAs) (gas microbubbles) adjacent to the BBB. These microbubbles (SonoVueTM, Bracco) were delivered via tail vein injection into the vasculature. To target the BBB, an ultrasonic transducer was suspended and focused through coupling gel onto the area of interest in the brain with skull the intact. The optimisation of this technique required determination of the focal position of the 3.5MHz transducer that was utilised, in addition to optimisation of the pulse length, pulse repetition frequency and power output of the ultrasound beam to enable the BBB to be disrupted. In addition, measurement of the attenuation of the ultrasound beam through ex vivo mouse skulls were measured. These results showed a 50% reduction in pressure amplitude from the baseline of 335.2mV (Baseline mean = 100% +/-SEM 0 n=3 (No skull), five regions across the skull averaged 47.79% +/-SEM 1.913 n=25 (using 5 different animals). In in vivo mice, after co-injection of the microbubbles with Evans Blue and insonation of the brain, disruption of the BBB was confirmed by the presence of Evans Blue dye in the brain, with no measurable damage occurring in the brain. This was confirmed by cell and nuclear morphology with no red blood cell extravasation into the surrounding tissue. The parameters used to open the BBB used a peak negative pressure of 2.1MPa (single pulse), transducer frequency 3.5MHz, 35,000 cycles over a 10ms burst at a pulse repetition frequency of 10Hz. The technique when applied in vivo in recovery animals is speculated to work by the focused ultrasound causing the microbubbles to oscillate within the vasculature adjacent to the BBB, resulting in high-shear stresses being generated on the tight junctions within the BBB. The resultant gaps in the BBB allow free circulating compounds (e.g. large dye molecules (Evans Blue - 960.8g/mol molecular weight) and adeno-associated-viruses (25nm with a packing capacity of 4.5kb) within the blood to pass into the brain, but there is no penetration of red blood cells (7μm). Longitudinal mouse experiments demonstrated that within 12-hours these gaps close with no long-term damage observed. Currently, utilising this technique, successful passage of an adeno-associated virus expressing GFP (as a marker) has been shown to pass into the brain (n=6 for each cohort including control) - indicating that the virus requires the ultrasound and microbubbles to facilitate its movement into the brain. Further technique optimisation is being explored looking at the role of CAs used in the opening and disruption of the BBB, comparing composition and size of the CAs. Microbubbles (2-3μm) and nanobubbles (200nm) were compared as well as lipid and non-ionic surfactant surface compositions, using volume of drug delivery and degree of disruption as outputs. Using this technique, the hydrophilic drug mimic calcein was delivered into the brain (n=5 non-ionic surfactant nanobubble, n=5 lipid nanobubble). Results have indicated that the delivery of calcein is most efficient when using non-ionic surfactant nanobubbles as opposed to lipid nanobubbles - with a greater volume of the drug being delivered into the cerebral tissue. Furthermore, the concentration and surface composition of the nanobubble have an effect as to the size and potential damage to the brain when opening the BBB. In conclusion, it has been shown that it is possible to non-invasively open the BBB and deliver viruses and dye into the brain. In addition, this thesis has investigated the use of nanobubbles as both facilitators to opening the BBB and delivery vectors for potentially therapeutic drugs. Finally, a non-invasive opening of the BBB has been achieved using focused ultrasound. Ultimately this non-invasive opening of the BBB can be used to achieve delivery of larger molecules (such as antibodies and viruses) into the brain to target treatments. Focused ultrasound brain targeting can be applied to the potential treatment of salt appetite regulation in the NTS. For the individuals who suffer from salt sensitive hypertension, the NTS can be targeted to reduce the drive to ingest high salt diets. Furthermore, the continuation of research into the central control of BP, salt appetite and baroreceptor reflex control can become better understood, using less invasive delivery techniques to the brain.

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Schiffman, Sara. « Sodium (Na) Levels in Drinking Water (H20) and Development of Hypertension in Children ». Honors in the Major Thesis, University of Central Florida, 2013. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/962.

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This integrative review of the literature focused on sodium (Na) content in drinking water (H?O) supplies and the subsequent effect on blood pressure levels in children. Studies for this review were drawn from the Cumulative Index of Nursing and Allied Health, PubMED, Science and Technology Databases, PsychInfo, United States (US) Environmental Protection Agency (EPA) and EPA in Florida websites. Criterion for inclusion in the data base searches were hypertension, high blood pressure, sodium in drinking water, drinking water salinity, children or preg'. Subsequently, further article selection criteria included children (under 18 years of age) and published in the English language (N=59). Findings of the review as summarized in this thesis could guide nursing research, education, policy and practice related to primary, secondary and tertiary interventions associated with sodium levels in drinking as a contributing factor to blood pressure levels in children.
B.S.N.
Bachelors
Nursing
Nursing

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Hiavacova, Alexandra. « Enhanced adrenergic sensitivity of mesenteric veins comparied to arteries and its relation to calcium utilization and handling ». Diss., Connect to online resource - MSU authorized users, 2008.

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Thesis (Ph.D.)--Michigan State University. Dept. of Pharmacology and Toxicology, 2008.
Title from PDF t.p. (viewed on July 10, 2009) Includes bibliographical references (p. 226-256). Also issued in print.

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Zanoli, Luca Maria. « Inflammation and arterial stiffness ». Doctoral thesis, Università di Catania, 2012. http://hdl.handle.net/10761/1088.

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Arterial stiffness is one of the earliest detectable manifestations of adverse structural and functional changes within the vessel wall. It is well known that increased large artery stiffness independently predicts the cardiovascular risk in a variety of populations. The identification of populations at higher risk of increased arterial stiffness and the knowledge of the mechanisms involved in arterial stiffening may help to identificate pharmacological and other treatments to reduce the arterial stiffness and improve the outcome of the patients. Recently, new advances have been proposed about the active role of inflammation and endothelial dysfunction in arterial stiffening and early atherosclerosis. The aims of this thesis were to review the literature and to study, for the first time, the arterial stiffness in inflammatory bowel disease.

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Pelazza, Bruno Bordin. « Comparação entre os valores da pressão arterial sistêmica central e braquial em mulheres e homens idosos com hipertensão arterial sistêmica ». Universidade Federal de Uberlândia, 2017. https://repositorio.ufu.br/handle/123456789/20992.

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Fundamentos: A pressão arterial sistêmica (PAS) se modifica com o envelhecimento. A PAS central apresenta correlação mais forte com os fatores de riscos cardiovasculares do que a PAS braquial. Nos idosos, o enrijecimento arterial progressivo e a onda de reflexão precoce, desenvolvem à amplificação da pressão de pulso (PP), em consequência da elevação da pressão arterial sistólica (PS). A mortalidade por doenças cardiovasculares em mulheres na pós-menopausa, apresenta prevalência igual ou superior aos homens, devido aos baixos níveis de estrogênio plasmático. Objetivo: Comparar os valores da pressão arterial sistêmica central e braquial entre mulheres e homens acima de 60 anos de idade portadores (as) de hipertensão arterial sistêmica. Métodos: Estudo quantitativo, descritivo, transversal, com pacientes idosos admitidos e selecionados a partir da demanda espontânea e programada nas unidades básicas de saúde de Uberlândia-MG, entre março de 2013 a março de 2014. Foram incluídos 69 participantes da pesquisa e comparamos a PAS central e braquial através do equipamento Sphygmocor® XCEL (AtCor Medical, Sydney, Austrália). Resultados: Houveram diferenças significantes nos valores pressóricos de toda a população tanto na PS central vs braquial 140(21) vs 153(23), mmHg quanto na PP central vs braquial 55(18) vs 70(18), mmHg. Além disso, o sexo feminino apresentou níveis pressóricos maiores do que no masculino, PS central 144(23) vs 134(16), mmHg e braquial 161(26) vs 148(18), mmHg, PP central 62(17) vs 45(14), mmHg e braquial 80(21) vs 63(15), mmHg, e isso foi significante. Conclusão: Portanto, houve diferenças significantes nos valores pressóricos da PS e PP, tanto a nível central quanto braquial em idosos hipertensos, observados na população total do estudo e entre mulheres e homens.
Background: Systemic arterial pressure (SBP) changes with aging. Central SBP has a stronger correlation with cardiovascular risk factors than brachial SBP. In the elderly, progressive arterial stiffness and the early reflection wave develop to the amplification of the pulse pressure (PP), as a consequence of the elevation of the systolic blood pressure (SP). Mortality due to cardiovascular diseases in postmenopausal women has a prevalence equal to or higher than men due to low levels of estrogen plasma. Objective: To compare the values of central and brachial systemic arterial pressure among women and men over 60 years of age with systemic arterial hypertension. Methods: A quantitative, descriptive, cross-sectional study with elderly patients admitted and selected from the spontaneous and programmed demand at the basic health units of Uberlândia-MG, between March 2013 and March 2014. We included 69 participants from the study and compared the Central and brachial PAS through the Sphygmocor® XCEL equipment (AtCor Medical, Sydney, Australia). Results: There were significant differences in the SP values of the entire population in the central SP vs the brachial SP 140 (21) vs 153 (23), mmHg and in the central PP vs brachial 55 (18) vs 70 (18), mmHg. Furthermore, females presented higher blood pressure levels than males, central SP 144 (23) vs 134 (16), mmHg and brachial 161 (26) vs 148 (18), mmHg, central PP 62 (17) vs 45 (14), mmHg and brachial 80 (21) vs 63 (15), mmHg, and this was significant. Conclusion: There were therefore significant differences in SP and PP pressure, both at the central and brachial levels in hypertensive elderly, observed in the total study population and between women and men.
Tese (Doutorado)

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Mounger, David Kyle, Kynlee Hillard, Brooke Tipton, Grayson D. White et Matthew R. Zahner. « GLP-1 agonist liraglutide increases metabolic- and cardiovascular-related sympathetic activity of the central nervous system ». Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/58.

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Metabolic syndrome is associated with pathologies that include type 2 diabetes, hypertension, and dyslipidemia, all of which increase the risks of heart disease. Glucagon-like peptide (GLP-1) is a hormone produced by intestinal enteroendocrine L‑cells. GLP-1 increases insulin sensitivity, augments glucose-dependent insulin secretion, and suppresses glucagon release. GLP-1 also works centrally to decrease appetite and increase metabolism. Evidence suggests that the beneficial effect is mediated by metabolically related sympathetic neurons within the hypothalamus. Although the hypothalamus contains neurons that control metabolism, there are also neurons that control cardiovascular activity. Considering that one main goal of obesity and diabetes treatments is to reduce cardiovascular-related comorbidities, any drug‑induced increase in blood pressure is unacceptable. Therefore, a better understanding of GLP-1 agonists on sympathetic activity and the role of the hypothalamus in central GLP‑1 activity is essential. In this study, we tested the hypothesis that the long‑acting FDA approved GLP-1 receptor agonist liraglutide activates both metabolic and cardiovascular‑related hypothalamic neurons and augments reflex cardiovascular sympathetic activity in rats. To test this hypothesis, we administered liraglutide (125 mg/kg, SC, n=10) or vehicle (saline, n=10) to rats for 15 days and measured food intake and body weight. Next, we recorded blood pressure and renal sympathetic nerve activity (RSNA) in the anesthetized rat before and after liraglutide treatment. Finally, to determine the activation of hypothalamic neurons we performed neuroanatomical tracing studies and turned metabolically-related (raphe‑projecting) neurons green, and cardiovascular-related (rostroventrolateral medulla, RVLM) neurons red. After treating rats with liraglutide, (75 mg/kg IV) we performed immunohistochemical (IHC) labeling to identify neurons expressing cFos, a marker of neuronal activation. Daily liraglutide significantly (p < 0.05) reduced both food intake and body weight from the pretreatment baseline. In vehicle-treated rats, the mean baseline food intake was 27.9 ± 0.5g. During vehicle treatment, the mean food intake was 28.6 ± 0.8 g and body weight was 110 ± 1.5% of its baseline. In liraglutide-treated rats, the mean baseline food intake was 29.9 ± 0.7g. During liraglutide treatment, the mean food intake was 22.7 ± 1.4g and body weight was 105 ± 1.1% of its baseline. At the end of liraglutide treatment, food intake and body weight returned to that of the vehicle-treated rats. In the anesthetized rat, liraglutide significantly (p < 0.05) increased basal RSNA and augmented baroreflex and chemoreflex activity. Lastly, our cFos data show that liraglutide activates metabolic, but not cardiovascular hypothalamic neurons. Collectively, these data suggest that although liraglutide elevates sympathetic activity, it is not by activation of pre-sympathetic hypothalamic neurons.

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Brink-Elfegoun, Thibault. « Limitations of maximal oxygen uptake during whole-body exercise / ». Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/20071116brin/.

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Pawelczyk, James A. (James Anthony). « Interactions between Carotid and Cardiopulmonary Baroreceptor Populations in Men with Varied Levels of Maximal Aerobic Power ». Thesis, University of North Texas, 1989. https://digital.library.unt.edu/ark:/67531/metadc331205/.

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Reductions in baroreflex responsiveness have been thought to increase the prevalence of orthostatic hypotension in endurance trained athletes. To test this hypothesis, cardiovascular responses to orthostatic stress, cardiopulmonary and carotid baroreflex responsiveness, and the effect of cardiopulmonary receptor deactivation on carotid baroreflex responses were examined in 24 men categorized by maximal aerobic power (V02max) into one of three groups: high fit (HF, V0-2max=67.0±1.9 ml•kg^-1•min^-1), moderately fit (MF, V0-2max=50.9±1.4 ml•kg^-1•min^-1), and low fit (LF, V0-2max=38.9±1.5 ml•kg^-1•min^-1). Orthostatic stress was induced using lower body negative pressure (LBNP) at -5, -10, -15, -20, -35, and -50 torr. Cardiopulmonary baroreflex responsiveness was assessed as the slope of the relationship between forearm vascular resistance (FVR, strain gauge plethysmography) and central venous pressure (CVP, dependent arm technigue) during LBNP<-35 torr. Carotid baroreflex responsiveness was assessed as the change in heart rate (HR, electrocardiography) or mean arterial pressure (MAP, radial artery catheter) elicited by 600 msec pulses of neck pressure and neck suction (NP/NS) from +40 to -70 torr. Pressures were applied using a lead collar wrapped about the subjects' necks during held expiration. Stimulus response data were fit to a logistic model and the parameters describing the curve were compared using two-factor ANOVA. The reductions CVP, mean (MAP), systolic, and pulse pressures during LBNP were similar between groups (P<0.05). However, diastolic blood pressure increased during LBNP m all but the HF group. (P<0.05). The slope of the FVR/CVP relationship did not differ between groups, nor did the form of the carotid-cardiac baroreflex stimulus response curve change during LBNP. changes in HR elicited with NP/NS were not different between groups (£>0.05). The range of the MAP stimulus response curve, however, was significantly less in the HP group compared to either the MP or LF group (£<0.05). These data imply that carotid baroreflex control of HR is unaltered by endurance exercise training, but carotid baroreflex control of blood pressure is impaired significantly, predisposing athletes to faintness.

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au, K. Powers-Martin@murdoch edu, et Kellysan Powers-Martin. « Nitric oxide and central autonomic control of blood pressure : A neuroanatomical study of nitric oxide and cGMP expression in the brain and spinal cord ». Murdoch University, 2008. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20090220.204446.

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Essential hypertension is defined as a chronic elevation of blood pressure of unknown cause. Though a definitive trigger for this change in blood pressure has not been established, there is a strong association with an upregulation of sympathetic output from the central nervous system. There are a number of central autonomic nuclei involved in the maintenance of blood pressure, including the brainstem regions of the nucleus tractus solitarii (NTS), caudal ventrolateral medulla (CVLM), rostral ventrolateral medulla (RVLM), the sympathetic preganglionic neurons (SPNs) within the intermediolateral cell column (IML) of the spinal cord, as well as forebrain regions such as the paraventricular nucleus (PVN) of the hypothalamus. Within these centers, a vast number of neurotransmitters have been identified that contribute to the control of blood pressure, including glutamate, angiotensin II, serotonin, neurotensin, neuropeptide Y, opioids and catecholamines. Recognition of the role of nitric oxide (NO) and its multiple influences over the neural control of blood pressure is gaining increasing significance. Nitric oxide is a unique modulatory molecule that acts as a non-conventional neurotransmitter. As NO is a gas with a short half-life of 4 6 seconds, its synthesising enzyme, nitric oxide synthase (NOS) is often used as a marker of location of production. Once activated, the best-known receptor for NO is soluble guanylate cyclase (sGC), which drives the production of cyclic guanosine monophosphate (cGMP). Identifying the presence of cGMP can therefore be used to determine sites receptive to NO. Previous studies examining the role of NO in the central autonomic control of blood pressure have focused predominantly upon application of either excitatory or inhibitory drugs into the key central autonomic regions and assessing pressor or depressor effects. This thesis aims instead to study the neuroanatomical relationship and functional significance of NO and cGMP expression in the brain and spinal cord of a hypertensive and normotensive rat model. In the first experimental chapter (Chapter 3), a comparative neuroanatomical analysis of neuronal NOS expression and its relationship with cGMP in the SPN of mature Spontaneously Hypertensive Rats (SHR) and their controls, Wistar Kyoto (WKY) was undertaken. Fluorescence immunohistochemistry confirmed the expression of nNOS in the majority of SPN located within the IML region of both strains. However, a strain specific anatomical arrangement of SPN cell clusters was evident and while there was no significant difference between the total number of SPN in each strain, there were significantly fewer nNOS positive SPN in the SHR animals. All nNOS positive SPN were found to express cGMP, and a novel subpopulation of nNOS negative, cGMP-positive SPN was identified. These cells were located in the medial edge of the IML SPN cell group. These results suggest that cGMP is a key signalling molecule in SPN, and that a reduced number of nNOS positive SPN in the SHR may be associated with the increase in sympathetic tone seen in essential hypertension. The second experimental chapter (Chapter 4) aimed to determine if reduced numbers of nNOS containing SPN translated into reduced detectable cGMP. The functional significance of cGMP signalling in the two strains was then examined. Based on previous work by our group, it was predicted that reduced nNOS in the SHR would translate into reduced cGMP and that intrathecal administration of exogenous cGMP in the spinal cord would drive a differential pressor response in the two animal strains. Immunohistochemical techniques confirmed that within each SPN, the relative level of cGMP expression was significantly reduced in the SHR when compared to the WKY. Intrathecal application of 8-bromo-cGMP, a drug analogous to cGMP, increased blood pressure in both strains and had a differential and dose dependent effect, causing only a small increase in blood pressure in anaesthetised WKY animals, while driving a significant pressor response in the SHR. This finding raised the novel hypothesis that in the SHR, reduced nNOS expression is not a driver of hypertension, but is instead a protective mechanism limiting the potent pressor effects of cGMP within SPN. The third experimental chapter (Chapter 5) examines the expression of neuronal and inducible isoforms of NOS (nNOS, iNOS) within the RVLM of SHR and WKY rats. Reverse transcription-polymerase chain reaction (RT-PCR) was used to analyse the level of mRNA expression and immunohistochemistry was then used to further analyse protein levels of nNOS. Total RNA was extracted and reverse transcribed from the RVLM of mature male WKY and SHR. Quantitative real-time PCR indicated that relative to WKY, mRNA levels for nNOS was significantly higher in RVLM of the SHR. This was confirmed immunohistochemically. When compared to iNOS, nNOS was expressed at significantly higher levels overall, however there was no difference in iNOS mRNA expression between the two strains. This demonstration of differential expression levels of nNOS and iNOS in the RVLM raises the possibilities that (i) NO production is up-regulated in the RVLM in SHR in response to increased sympathetic activity in order to re-establish homeostatic balance or alternatively that (ii) an alteration in the balance between nNOS and iNOS activity may underlie the genesis of augmented sympathetic vasomotor tone during hypertension. The fourth experimental chapter (Chapter 6) extends the observations in Chapter 5 through examination of the expression of cGMP and sGC within the RVLM. There is strong functional evidence to suggest that NO signalling in the RVLM relies on cGMP as an intracellular signalling molecule and that this pathway is impaired in hypertension. Immunohistochemistry was used to assess cGMP expression as a marker of active NO signalling in the C1 region of the RVLM, again comparing SHR and WKY animals. Fluorescence immunohistochemistry on sections of the RVLM, double labelled for cGMP and either nNOS or phenylethylamine methyl-transferase (PNMT) failed to reveal cGMP positive neurons in the RVLM from aged animals of either strain, despite consistent detection of cGMP immunoreactivity neurons in the nucleus ambiguus from the same or adjacent sections. This was demonstrated both in the presence and absence of the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) and in young vs. aged animals. In-vitro incubation of RVLM slices in the NO donor DETA-NO or NMDA did not reveal any additional cGMP neuronal staining within the RVLM. In all studies, cGMP was prominent within the vasculature. Soluble guanylate cyclase immunoreactivity was found throughout the RVLM, although it did not co-localise with the PNMT or nNOS neuronal populations. Overall, results suggest that within the RVLM, cGMP is not detectable in the resting state and cannot be elicited by phosphodiesterase inhibition, NMDA receptor stimulation or NO donor application. A short time course of cGMP signalling or degradation not inhibited by the phosphodiesterase inhibitor utilised (IBMX) in the RVLM cannot be excluded. The final experimental chapter (Chapter 7) examines cGMP expression in magnocellular and preautonomic parvocellular neurons of the PVN. Retrograde tracing techniques and immunohistochemistry were used to visualise cGMP immunoreactivity within functionally, neurochemically and topographically defined PVN neuronal populations in Wistar rats. Basal cGMP immunoreactivity was readily observed in the PVN, both in neuronal and vascular profiles. Cyclic GMP immunoreactivity was significantly higher in magnocellular compared to preautonomic neuronal populations. In preautonomic neurons, the level of cGMP expression was independent on their subnuclei location, innervated target or neurochemical phenotype. The data presented in this chapter indicates a highly heterogeneous distribution of basal cGMP levels within the PVN, and supports work by others indicating that constitutive NO inhibitory actions on preautonomic PVN neurons are likely mediated indirectly through activation of interneurons. Summary Together, these studies comprise a detailed analysis of the neuroanatomical expression of NO and its signalling molecule cGMP in key central autonomic regions involved in the regulation of blood pressure. Under resting or basal conditions, the studies demonstrate notable differences in the expression of NO synthesising enzymes between normotensive and hypertensive animals, and correlating changes in the downstream signalling molecule cGMP. In the spinal cord, novel functional differences in cGMP activity were also demonstrated. In the RVLM, although differences in nNOS were demonstrated, cGMP expression could not be readily detected in either the WKY or SHR, while in contrast within the PVN, cGMP was detected in both magnocellular and parvocellular neuronal populations. Conclusion This thesis gives insight into the physiological role of NO and cGMP as mediators of central blood pressure control. The results presented indicate that the NO-cGMP dependent signalling pathway may not be the dominant driver responsible for maintaining high blood pressure in the SHR model of essential hypertension, and that there is no globally consistent pattern of expression, and indeed the role of NO as a mediator of pressor and depressor function may vary between the autonomic regions examined. Further, it is possible that this pathway is only recruited during activation of reflex homeostatic pathways or during times of marked physiological stress, and that the differences we see in basal expression between the normotensive and SHR animals are instead a result of compensatory mechanisms.

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32

Powers-Martin, Kellysan. « Nitric oxide and central autonomic control of blood pressure : a neuroanatomical study of nitric oxide and cGMP expression in the brain and spinal cord ». Thesis, Powers-Martin, Kellysan (2008) Nitric oxide and central autonomic control of blood pressure : a neuroanatomical study of nitric oxide and cGMP expression in the brain and spinal cord. PhD thesis, Murdoch University, 2008. https://researchrepository.murdoch.edu.au/id/eprint/483/.

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Essential hypertension is defined as a chronic elevation of blood pressure of unknown cause. Though a definitive trigger for this change in blood pressure has not been established, there is a strong association with an upregulation of sympathetic output from the central nervous system. There are a number of central autonomic nuclei involved in the maintenance of blood pressure, including the brainstem regions of the nucleus tractus solitarii (NTS), caudal ventrolateral medulla (CVLM), rostral ventrolateral medulla (RVLM), the sympathetic preganglionic neurons (SPNs) within the intermediolateral cell column (IML) of the spinal cord, as well as forebrain regions such as the paraventricular nucleus (PVN) of the hypothalamus. Within these centers, a vast number of neurotransmitters have been identified that contribute to the control of blood pressure, including glutamate, angiotensin II, serotonin, neurotensin, neuropeptide Y, opioids and catecholamines. Recognition of the role of nitric oxide (NO) and its multiple influences over the neural control of blood pressure is gaining increasing significance. Nitric oxide is a unique modulatory molecule that acts as a non-conventional neurotransmitter. As NO is a gas with a short half-life of 4 - 6 seconds, its' synthesising enzyme, nitric oxide synthase (NOS) is often used as a marker of location of production. Once activated, the best-known 'receptor' for NO is soluble guanylate cyclase (sGC), which drives the production of cyclic guanosine monophosphate (cGMP). Identifying the presence of cGMP can therefore be used to determine sites receptive to NO. Previous studies examining the role of NO in the central autonomic control of blood pressure have focused predominantly upon application of either excitatory or inhibitory drugs into the key central autonomic regions and assessing pressor or depressor effects. This thesis aims instead to study the neuroanatomical relationship and functional significance of NO and cGMP expression in the brain and spinal cord of a hypertensive and normotensive rat model. In the first experimental chapter (Chapter 3), a comparative neuroanatomical analysis of neuronal NOS expression and its relationship with cGMP in the SPN of mature Spontaneously Hypertensive Rats (SHR) and their controls, Wistar Kyoto (WKY) was undertaken. Fluorescence immunohistochemistry confirmed the expression of nNOS in the majority of SPN located within the IML region of both strains. However, a strain specific anatomical arrangement of SPN cell clusters was evident and while there was no significant difference between the total number of SPN in each strain, there were significantly fewer nNOS positive SPN in the SHR animals. All nNOS positive SPN were found to express cGMP, and a novel subpopulation of nNOS negative, cGMP-positive SPN was identified. These cells were located in the medial edge of the IML SPN cell group. These results suggest that cGMP is a key signalling molecule in SPN, and that a reduced number of nNOS positive SPN in the SHR may be associated with the increase in sympathetic tone seen in essential hypertension. The second experimental chapter (Chapter 4) aimed to determine if reduced numbers of nNOS containing SPN translated into reduced detectable cGMP. The functional significance of cGMP signalling in the two strains was then examined. Based on previous work by our group, it was predicted that reduced nNOS in the SHR would translate into reduced cGMP and that intrathecal administration of exogenous cGMP in the spinal cord would drive a differential pressor response in the two animal strains. Immunohistochemical techniques confirmed that within each SPN, the relative level of cGMP expression was significantly reduced in the SHR when compared to the WKY. Intrathecal application of 8-bromo-cGMP, a drug analogous to cGMP, increased blood pressure in both strains and had a differential and dose dependent effect, causing only a small increase in blood pressure in anaesthetised WKY animals, while driving a significant pressor response in the SHR. This finding raised the novel hypothesis that in the SHR, reduced nNOS expression is not a driver of hypertension, but is instead a protective mechanism limiting the potent pressor effects of cGMP within SPN. The third experimental chapter (Chapter 5) examines the expression of neuronal and inducible isoforms of NOS (nNOS, iNOS) within the RVLM of SHR and WKY rats. Reverse transcription-polymerase chain reaction (RT-PCR) was used to analyse the level of mRNA expression and immunohistochemistry was then used to further analyse protein levels of nNOS. Total RNA was extracted and reverse transcribed from the RVLM of mature male WKY and SHR. Quantitative real-time PCR indicated that relative to WKY, mRNA levels for nNOS was significantly higher in RVLM of the SHR. This was confirmed immunohistochemically. When compared to iNOS, nNOS was expressed at significantly higher levels overall, however there was no difference in iNOS mRNA expression between the two strains. This demonstration of differential expression levels of nNOS and iNOS in the RVLM raises the possibilities that (i) NO production is up-regulated in the RVLM in SHR in response to increased sympathetic activity in order to re-establish homeostatic balance or alternatively that (ii) an alteration in the balance between nNOS and iNOS activity may underlie the genesis of augmented sympathetic vasomotor tone during hypertension. The fourth experimental chapter (Chapter 6) extends the observations in Chapter 5 through examination of the expression of cGMP and sGC within the RVLM. There is strong functional evidence to suggest that NO signalling in the RVLM relies on cGMP as an intracellular signalling molecule and that this pathway is impaired in hypertension. Immunohistochemistry was used to assess cGMP expression as a marker of active NO signalling in the C1 region of the RVLM, again comparing SHR and WKY animals. Fluorescence immunohistochemistry on sections of the RVLM, double labelled for cGMP and either nNOS or phenylethylamine methyl-transferase (PNMT) failed to reveal cGMP positive neurons in the RVLM from aged animals of either strain, despite consistent detection of cGMP immunoreactivity neurons in the nucleus ambiguus from the same or adjacent sections. This was demonstrated both in the presence and absence of the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) and in young vs. aged animals. In-vitro incubation of RVLM slices in the NO donor DETA-NO or NMDA did not reveal any additional cGMP neuronal staining within the RVLM. In all studies, cGMP was prominent within the vasculature. Soluble guanylate cyclase immunoreactivity was found throughout the RVLM, although it did not co-localise with the PNMT or nNOS neuronal populations. Overall, results suggest that within the RVLM, cGMP is not detectable in the resting state and cannot be elicited by phosphodiesterase inhibition, NMDA receptor stimulation or NO donor application. A short time course of cGMP signalling or degradation not inhibited by the phosphodiesterase inhibitor utilised (IBMX) in the RVLM cannot be excluded. The final experimental chapter (Chapter 7) examines cGMP expression in magnocellular and preautonomic parvocellular neurons of the PVN. Retrograde tracing techniques and immunohistochemistry were used to visualise cGMP immunoreactivity within functionally, neurochemically and topographically defined PVN neuronal populations in Wistar rats. Basal cGMP immunoreactivity was readily observed in the PVN, both in neuronal and vascular profiles. Cyclic GMP immunoreactivity was significantly higher in magnocellular compared to preautonomic neuronal populations. In preautonomic neurons, the level of cGMP expression was independent on their subnuclei location, innervated target or neurochemical phenotype. The data presented in this chapter indicates a highly heterogeneous distribution of basal cGMP levels within the PVN, and supports work by others indicating that constitutive NO inhibitory actions on preautonomic PVN neurons are likely mediated indirectly through activation of interneurons. Summary Together, these studies comprise a detailed analysis of the neuroanatomical expression of NO and its signalling molecule cGMP in key central autonomic regions involved in the regulation of blood pressure. Under resting or basal conditions, the studies demonstrate notable differences in the expression of NO synthesising enzymes between normotensive and hypertensive animals, and correlating changes in the downstream signalling molecule cGMP. In the spinal cord, novel functional differences in cGMP activity were also demonstrated. In the RVLM, although differences in nNOS were demonstrated, cGMP expression could not be readily detected in either the WKY or SHR, while in contrast within the PVN, cGMP was detected in both magnocellular and parvocellular neuronal populations. Conclusion This thesis gives insight into the physiological role of NO and cGMP as mediators of central blood pressure control. The results presented indicate that the NO-cGMP dependent signalling pathway may not be the dominant driver responsible for maintaining high blood pressure in the SHR model of essential hypertension, and that there is no globally consistent pattern of expression, and indeed the role of NO as a mediator of pressor and depressor function may vary between the autonomic regions examined. Further, it is possible that this pathway is only recruited during activation of reflex homeostatic pathways or during times of marked physiological stress, and that the differences we see in basal expression between the normotensive and SHR animals are instead a result of compensatory mechanisms.

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33

Powers-Martin, Kellysan. « Nitric oxide and central autonomic control of blood pressure : a neuroanatomical study of nitric oxide and cGMP expression in the brain and spinal cord ». Powers-Martin, Kellysan (2008) Nitric oxide and central autonomic control of blood pressure : a neuroanatomical study of nitric oxide and cGMP expression in the brain and spinal cord. PhD thesis, Murdoch University, 2008. http://researchrepository.murdoch.edu.au/483/.

Texte intégral

Résumé :

Essential hypertension is defined as a chronic elevation of blood pressure of unknown cause. Though a definitive trigger for this change in blood pressure has not been established, there is a strong association with an upregulation of sympathetic output from the central nervous system. There are a number of central autonomic nuclei involved in the maintenance of blood pressure, including the brainstem regions of the nucleus tractus solitarii (NTS), caudal ventrolateral medulla (CVLM), rostral ventrolateral medulla (RVLM), the sympathetic preganglionic neurons (SPNs) within the intermediolateral cell column (IML) of the spinal cord, as well as forebrain regions such as the paraventricular nucleus (PVN) of the hypothalamus. Within these centers, a vast number of neurotransmitters have been identified that contribute to the control of blood pressure, including glutamate, angiotensin II, serotonin, neurotensin, neuropeptide Y, opioids and catecholamines. Recognition of the role of nitric oxide (NO) and its multiple influences over the neural control of blood pressure is gaining increasing significance. Nitric oxide is a unique modulatory molecule that acts as a non-conventional neurotransmitter. As NO is a gas with a short half-life of 4 - 6 seconds, its' synthesising enzyme, nitric oxide synthase (NOS) is often used as a marker of location of production. Once activated, the best-known 'receptor' for NO is soluble guanylate cyclase (sGC), which drives the production of cyclic guanosine monophosphate (cGMP). Identifying the presence of cGMP can therefore be used to determine sites receptive to NO. Previous studies examining the role of NO in the central autonomic control of blood pressure have focused predominantly upon application of either excitatory or inhibitory drugs into the key central autonomic regions and assessing pressor or depressor effects. This thesis aims instead to study the neuroanatomical relationship and functional significance of NO and cGMP expression in the brain and spinal cord of a hypertensive and normotensive rat model. In the first experimental chapter (Chapter 3), a comparative neuroanatomical analysis of neuronal NOS expression and its relationship with cGMP in the SPN of mature Spontaneously Hypertensive Rats (SHR) and their controls, Wistar Kyoto (WKY) was undertaken. Fluorescence immunohistochemistry confirmed the expression of nNOS in the majority of SPN located within the IML region of both strains. However, a strain specific anatomical arrangement of SPN cell clusters was evident and while there was no significant difference between the total number of SPN in each strain, there were significantly fewer nNOS positive SPN in the SHR animals. All nNOS positive SPN were found to express cGMP, and a novel subpopulation of nNOS negative, cGMP-positive SPN was identified. These cells were located in the medial edge of the IML SPN cell group. These results suggest that cGMP is a key signalling molecule in SPN, and that a reduced number of nNOS positive SPN in the SHR may be associated with the increase in sympathetic tone seen in essential hypertension. The second experimental chapter (Chapter 4) aimed to determine if reduced numbers of nNOS containing SPN translated into reduced detectable cGMP. The functional significance of cGMP signalling in the two strains was then examined. Based on previous work by our group, it was predicted that reduced nNOS in the SHR would translate into reduced cGMP and that intrathecal administration of exogenous cGMP in the spinal cord would drive a differential pressor response in the two animal strains. Immunohistochemical techniques confirmed that within each SPN, the relative level of cGMP expression was significantly reduced in the SHR when compared to the WKY. Intrathecal application of 8-bromo-cGMP, a drug analogous to cGMP, increased blood pressure in both strains and had a differential and dose dependent effect, causing only a small increase in blood pressure in anaesthetised WKY animals, while driving a significant pressor response in the SHR. This finding raised the novel hypothesis that in the SHR, reduced nNOS expression is not a driver of hypertension, but is instead a protective mechanism limiting the potent pressor effects of cGMP within SPN. The third experimental chapter (Chapter 5) examines the expression of neuronal and inducible isoforms of NOS (nNOS, iNOS) within the RVLM of SHR and WKY rats. Reverse transcription-polymerase chain reaction (RT-PCR) was used to analyse the level of mRNA expression and immunohistochemistry was then used to further analyse protein levels of nNOS. Total RNA was extracted and reverse transcribed from the RVLM of mature male WKY and SHR. Quantitative real-time PCR indicated that relative to WKY, mRNA levels for nNOS was significantly higher in RVLM of the SHR. This was confirmed immunohistochemically. When compared to iNOS, nNOS was expressed at significantly higher levels overall, however there was no difference in iNOS mRNA expression between the two strains. This demonstration of differential expression levels of nNOS and iNOS in the RVLM raises the possibilities that (i) NO production is up-regulated in the RVLM in SHR in response to increased sympathetic activity in order to re-establish homeostatic balance or alternatively that (ii) an alteration in the balance between nNOS and iNOS activity may underlie the genesis of augmented sympathetic vasomotor tone during hypertension. The fourth experimental chapter (Chapter 6) extends the observations in Chapter 5 through examination of the expression of cGMP and sGC within the RVLM. There is strong functional evidence to suggest that NO signalling in the RVLM relies on cGMP as an intracellular signalling molecule and that this pathway is impaired in hypertension. Immunohistochemistry was used to assess cGMP expression as a marker of active NO signalling in the C1 region of the RVLM, again comparing SHR and WKY animals. Fluorescence immunohistochemistry on sections of the RVLM, double labelled for cGMP and either nNOS or phenylethylamine methyl-transferase (PNMT) failed to reveal cGMP positive neurons in the RVLM from aged animals of either strain, despite consistent detection of cGMP immunoreactivity neurons in the nucleus ambiguus from the same or adjacent sections. This was demonstrated both in the presence and absence of the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) and in young vs. aged animals. In-vitro incubation of RVLM slices in the NO donor DETA-NO or NMDA did not reveal any additional cGMP neuronal staining within the RVLM. In all studies, cGMP was prominent within the vasculature. Soluble guanylate cyclase immunoreactivity was found throughout the RVLM, although it did not co-localise with the PNMT or nNOS neuronal populations. Overall, results suggest that within the RVLM, cGMP is not detectable in the resting state and cannot be elicited by phosphodiesterase inhibition, NMDA receptor stimulation or NO donor application. A short time course of cGMP signalling or degradation not inhibited by the phosphodiesterase inhibitor utilised (IBMX) in the RVLM cannot be excluded. The final experimental chapter (Chapter 7) examines cGMP expression in magnocellular and preautonomic parvocellular neurons of the PVN. Retrograde tracing techniques and immunohistochemistry were used to visualise cGMP immunoreactivity within functionally, neurochemically and topographically defined PVN neuronal populations in Wistar rats. Basal cGMP immunoreactivity was readily observed in the PVN, both in neuronal and vascular profiles. Cyclic GMP immunoreactivity was significantly higher in magnocellular compared to preautonomic neuronal populations. In preautonomic neurons, the level of cGMP expression was independent on their subnuclei location, innervated target or neurochemical phenotype. The data presented in this chapter indicates a highly heterogeneous distribution of basal cGMP levels within the PVN, and supports work by others indicating that constitutive NO inhibitory actions on preautonomic PVN neurons are likely mediated indirectly through activation of interneurons. Summary Together, these studies comprise a detailed analysis of the neuroanatomical expression of NO and its signalling molecule cGMP in key central autonomic regions involved in the regulation of blood pressure. Under resting or basal conditions, the studies demonstrate notable differences in the expression of NO synthesising enzymes between normotensive and hypertensive animals, and correlating changes in the downstream signalling molecule cGMP. In the spinal cord, novel functional differences in cGMP activity were also demonstrated. In the RVLM, although differences in nNOS were demonstrated, cGMP expression could not be readily detected in either the WKY or SHR, while in contrast within the PVN, cGMP was detected in both magnocellular and parvocellular neuronal populations. Conclusion This thesis gives insight into the physiological role of NO and cGMP as mediators of central blood pressure control. The results presented indicate that the NO-cGMP dependent signalling pathway may not be the dominant driver responsible for maintaining high blood pressure in the SHR model of essential hypertension, and that there is no globally consistent pattern of expression, and indeed the role of NO as a mediator of pressor and depressor function may vary between the autonomic regions examined. Further, it is possible that this pathway is only recruited during activation of reflex homeostatic pathways or during times of marked physiological stress, and that the differences we see in basal expression between the normotensive and SHR animals are instead a result of compensatory mechanisms.

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34

Powers-Martin, Kellysan. « Nitric oxide and central autonomic control of blood pressure : a neuronatomical study of nitric oxide and cGMP expression in the brain and spinal cord / ». Murdoch University Digital Theses Program, 2008. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20090220.204446.

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35

Mendes, Alessandra Beatriz Balduino. « Avaliação da rigidez arterial e pressão aórtica central em pacientes hipertensos resistentes ». Faculdade de Medicina de São José do Rio Preto, 2015. http://hdl.handle.net/tede/268.

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Background: Hypertension Resistant (RH) is defined as office blood pressure (BP) ≥140 / 90 mmHg in patients using at least three antihypertensive classes at optimal doses, including a diuretic. Arterial stiffness is a major manifestation of RH, a determining fator, for increasing central pressure and pulse pressure. Arterial stiffness can be measured by three parameters: the central arterial pressure (CAP), augmentation index (AIx) and pulse wave velocity (PWV). These parameters can be estimated by simple methods, non-invasive and with high sensitivity, such as tonometry or 24-hour ambulatory blood pressure monitoring (ABPM). Objectives: To study and compare the anthropometric, biochemical profile and central hemodynamic values (CAP, AIx and PWV) by 24-hour ABPM in patients resistant hypertension (RH), controlled hypertensive (CH) and normotensive (NT). Methodology: We selected 59 patients with resistant hypertension, 62 controlled hypertensive and 60 normotensive, all submitted to ABPM. The level of significance was accepted for P-value <0.05. Results: Individuals CH and RH group presented higher mean age and higher body mass index (60.4; 60.2 years and 29.6; 29.7 kg/m2, respectively) compared to the NT group (53.2 years and 26.2 kg/m2) (P <0.05). RH showed higher levels of creatinine and decreased renal function (1.1 mg/dL and 67.3mL/min/m2) compared to CH (0.9 mg/dL and 79.3mL/min/m2, P <0.05) and NT (0.8 mg/dl and 85.3mL/min/m 2; P <0.05). Glucose and uric acid were higher and HDL-C lower in the RH group compared to CH and NT, but without statistical significance. Systolic blood pressure (SBP) and diastolic pressure (DBP) of office were significantly higher in the RH group (137.1/80.7mmHg) compared to CH (124.3/74.0mmHg) and NT (117.5/74.3mmHg). SBP and DBP in the 24-hour ABPM in daytime and night were higher in RH (129.4/78.9, 130/80 and 128.3/76.9mmHg, respectively) compared to CH (119.4/72.7; 121.3/75.0 and 115.7/68.3mmHg, respectively) and NT (114.8/71.8, 117.8/74.8 and 109.3/66.4mmHg, respectively). Heart rate (HR) and pulse pressure (PP) were significantly higher in RH (72.4bpm/min and 52.2mmHg, respectively) than in groups CH (67.5bpm/min and 47.2mmHg, respectively) and NT (67.3bpm/min and 42.9mmHg, respectively) during the sleep period. RH showed less nocturnal than CH and NT (P <0.05). SBP and DBP in the 24-hour ABPM in daytime and night were significantly higher in RH (119.2, 118.8 and 119.8mmHg, respectively) compared to CH (110.4, 111.5 and 109mmHg, respectively) and NT (107.2; 109.2 and 104.2mmHg, respectively). PWV was higher in RH compared to CH and NT diring the three periods assessed, although there was no statistical significance. The AIx values did not differ among the three groups in all periods. In RH, age and PWV were significantly associated to the CAP. There was a positive correlation between central SBP and PP and between central SBP and PWV in the RH group. Conclusion: The patients with resistant hypertension presented CAP_ higher level than the ones with controlled hypertensive and normotensive; this clearly demonstrates a greater arterial stiffness and a growing cardiovascular risk.
Introdução: A Hipertensão Arterial Resistente (HAR) é definida por pressão arterial (PA) de consultório ≥140/90 mmHg, em paciente usando, pelo menos, três classes de anti-hipertensivos em dosagens otimizadas, incluindo um diurético. A rigidez arterial é uma das principais manifestações da HAR e é determinante para o aumento da pressão arterial central (PAC) e de pulso (PP). A rigidez arterial pode ser avaliada por três parâmetros: pressão arterial central (PAC), augmentation index (AIx) e velocidade de onda de pulso (VOP). Esses parâmetros podem ser estimados por métodos simples, não invasivos e com boa sensibilidade, tais como, a tonometria de aplanação ou a monitorização ambulatorial da pressão arterial (MAPA) de 24 horas. Objetivos: Estudar e comparar o perfil antropométrico, bioquímico e os valores de hemodinâmica central (PAC, AIx e VOP) por meio da MAPA 24 horas em hipertensos resistentes (HR), hipertensos controlados (HC) e normotensos (NT). Metodologia: Foram selecionados 59 pacientes hipertensos resistentes, 62 hipertensos controlados e 60 normotensos; todos submetidos à MAPA. O nível de significância admitido foi para valor-P<0,05. Resultados: Indivíduos do grupo HC e HR tiveram maior média de idade e maior índice de massa corpórea (60,4; 60,2 anos e 29,6; 29,7 Kg/m2, respectivamente) em relação ao grupo NT (53,2 anos e 26,2 Kg/m2) (P<0,05). HR apresentaram maior nível de creatinina e de redução da função renal (1,1mg/dL e 67,3mL/min/m2) comparados ao HC (0,9mg/dL e 79,3mL/min/m2; P<0,05) e NT (0,8mg/dL e 85,3mL/min/m2; P<0,05). Glicemia e ácido úrico foram maiores e HDL-c menor no grupo HR em comparação aos HC e NT, mas sem significância estatística. Pressão arterial sistólica (PAS) e diastólica (PAD) de consultório foram significantemente maiores no grupo HR (137,1/80,7 mmHg) quando comparados ao HC (124,3/74 mmHg) e NT (117,5/74,3 mmHg). PAS e PAD na MAPA 24h, na vigília e no sono foram maiores em HR (129,4/78,9; 130/80 e 128,3/76,9 mmHg, respectivamente) em comparação ao HC (119,4/72,7; 121,3/75 e 115,7/68,3 mmHg, respectivamente) e NT (114,8/71,8; 117,8/74,8 e 109,3/66,4 mmHg, respectivamente). Frequência cardíaca (FC) e pressão de pulso (PP) foram significantemente mais elevadas no HR (72,4 bpm/min e 52,2 mmHg, respectivamente) do que nos grupos HC (67,5 bpm/min e 47,2 mmHg, respectivamente) e NT (67,3 bpm/min e 42,9 mmHg, respectivamente) durante o período de sono. HR apresentaram menor descenso noturno do que HC e NT (P<0,05). PAS central de 24h, na vigília e no sono foram significantemente maiores nos HR (119,2; 118,8 e 119,8 mmHg, respectivamente) comparadas aos HC (110,4; 111,5 e 109 mmHg, respectivamente) e NT (107,2; 109,2 e 104,2 mmHg, respectivamente). VOP foi maior no HR em comparação a HC e NT nos três períodos avaliados, apesar de não haver significância estatística. Os valores de AIx não apresentaram diferença entre os três grupos em todos os períodos. Em HR, a idade e a VOP foram significantemente associadas à PAC. Houve correlação positiva entre PAS central e PP e entre PAS central e VOP no grupo HR. Conclusão: Hipertensos resistentes apresentaram maior nível de PAC do que hipertensos controlados e normotensos; fato que demonstra maior rigidez arterial nesse grupo e, consequentemente, maior risco cardiovascular.

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36

RAMOS, BECERRA CARLOS GERARDO. « Pulse wave for analysis : comparation of data obtained with different methods ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2011. http://hdl.handle.net/10281/20692.

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Background Central aortic blood pressure has received in recent years more interest as a more accurate predictor of outcome than brachial artery blood pressure. Number of techniques exists to assess the aortic pressure. Objetive To compare the values of central systolic pressure and peripheral augmentation index in hypertensive patients calculated by the Omron and the SphygmoCor systems. Methods Eighty-four (84) hypertensive subjects (40 males and 44 females), mean aged 58 ± 12 years were examined at the Hypertension Unit at San Luca Hospital (Istituto Auxologico Italiano) Milan Italia. All 84 subjects were treated with antihypertensive therapy. Results Statistics Data were analyzed using Statistica software version 9.0 (StatSoft Tulsa, Oklahoma. Inc). Pearson product–moment correlation coefficient (r) was used to determine associations between variables. Bland–Altman plots were used to assess agreement between methods. Dependent t tests were used to compare means. 1) Comparison between central pressure values provided by Sphygmocor and by Omron. There was a good correlation between cSBPsphy and cSBPomr (r=0.76; r²=58, P=< 0.001), but with a mean difference of -16 ± 13 mmHg, indicating a systematic underestimation by Omron device. 2) Comparison between cSBPsphy and pSBP2omr values showed also a good correlation, r= 0.74; r²=55, P <0.001, with a mean difference of only -0.8 ± 13 mmHg, indicating a good mean agreement. 3) Peripheral augmentation index measured by both devices showed close correlation (r=0.66; r²= 43 P < 0.001) but a mean difference Sphy-Omr of 62 ± 19, indicating important overestimation by the Sphygmocor. Discussion When comparing the original pSBP2omr values with the cSBP calculated by SphygmoCor, the mean difference was only -0.8 ± 13 mmHg. Direct invasive measurements of aortic pressure must be developed for a better algorithm to convert pSBP2omr to cSBPomr. Peripheral augmentation index is calculated by the same formula in both devices, there was a good correlation between the values of pAIx calculated by each device (r=0.66; r²= 0.43, P=< 0.001), but a very poor agreement. In summary estimated cSBP provided by the Omron system good correlation and limited agreement with values obtained from the SphygmoCor system. Conversely cSBP with Sphygmocor showed good agreement with pSBP2 measured by OMRON. Further investigations should compare estimates of pSBP2 by the Omron system to direct measurements of aortic pressure by cardiac catheterisation. The results suggest that the Omron system has an accurate of pSBP2 which show strong correlations with those of the SphygmoCor device.

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Fonseca, Sueli Ferreira da. « Participa??o do sistema colin?rgico central na modula??o das respostas cardiovasculares e termorregulat?rias em ratos espontaneamente hipertensos ». UFVJM, 2017. http://acervo.ufvjm.edu.br/jspui/handle/1/1745.

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Existem evid?ncias que a estimula??o colin?rgica central aumenta a dissipa??o de calor em ratos normotensos como consequ?ncia de altera??es cardiovasculares via modula??o da atividade barorreflexa. No entanto, n?o h? dados publicados sobre o envolvimento do sistema colin?rgico central nestas respostas em modelo experimental que apresenta altera??o da sensibilidade dos barorreceptores e d?ficit termorregulat?rio. Assim, o objetivo do presente estudo foi verificar o envolvimento do sistema colin?rgico central na modula??o das repostas cardiovasculares e termorregulat?rias durante o repouso e exerc?cio f?sico em ratos espontaneamente hipertensos (SHR). Ratos Wistar machos (n = 33) e SHR (n = 33) foram implantados com uma c?nula intracerebroventricular (icv) para inje??es de 2 ?L de fisostigmina (fis) ou solu??o salina (sal). Temperaturas da cauda (Tcauda) e corporal interna (Tint), press?o arterial sist?lica (PAS), frequ?ncia card?aca (FC) e taxa metab?lica foram registradas durante os 60 minutos em que os ratos permaneceram em repouso, bem como durante o exerc?cio f?sico at? a fadiga ap?s inje??es icv randomizadas. Na situa??o repouso, o tratamento com fis iniciou uma sucess?o de respostas cardiovasculares e termorregulat?rias que resultaram em aumento da PAS, redu??o da FC e aumento de Tcauda nos grupos Wistar e SHR. A magnitude da ativa??o desses mecanismos foi mais intensa no SHR, afetando a Tint e melhorando a dissipa??o de calor. Durante o exerc?cio f?sico, o tratamento com fis foi capaz de modular as repostas cardiovasculares promovendo aumento significativo da PAS, seguido de bradicardia reflexa em ratos SHR e Wistar. Estas respostas foram mais intensas nos ratos Wistar. N?o houve diferen?a significativa para a Tcauda e Tint no grupo SHR fis em rela??o ao grupo sal. Entretanto, fis impactou positivamente no desempenho f?sico. Em conjunto, esses resultados fornecem evid?ncias que, durante a situa??o de repouso, a estimula??o colin?rgica central modula as repostas termorregulat?rias por meio de mudan?as no sistema cardiovascular de ratos Wistar e SHR, sendo que essas respostas s?o mais acentuadas em ratos SHR impactando na dissipa??o de calor. Durante o exerc?cio f?sico, a administra??o central de fis promove altera??es no sistema cardiovascular de ratos normotensos e hipertensos. Apesar dessas altera??es n?o terem sido suficientes para ajustar as respostas termorregulat?rias em ratos SHR, impactaram positivamente no desempenho f?sico.
Tese (Doutorado) ? Programa Multic?ntrico de P?s-Gradua??o em Ci?ncias Fisiol?gicas, Universidade Federal dos Vales do Jequitinhonha e Mucuri, 2017.
There is evidence that central cholinergic stimulation increases heat dissipation in normotensive rats through changes on the cardiovascular system via modulation of baroreceptors function. However, there is no published data regarding the involvement of the central cholinergic system in cardiovascular and thermoregulatory responses in spontaneously hypertensive rats (SHR), which are animals that possess altered baroreceptor sensitivity and thermoregulatory deficit. Therefore, the aim of this study was to verify the involvement of the central cholinergic system in cardiovascular and thermoregulatory adjustments in SHR. Male Wistar (n = 33) and SHR (n = 33) rats were implanted with an intracerebroventricular (icv) cannula for injections of 2 ?L of physostigmine (phy) or saline (sal) solution. Tail (Ttail) and internal body temperatures (Tint), systolic arterial pressure (SAP), heart rate (HR) and metabolic rate were registered during 60 minutes while the animals remained at rest and during exercise until fatigue after randomly receiving the injections. Phy treatment started a succession of cardiovascular and thermoregulatory responses that resulted in increased SAP, reduced HR and increased Ttail in both Wistar and SHR groups. The magnitude of the activation of these mechanisms seems to be more intense in SHR, even affecting the Tint, and improve heat dissipation. During physical exercise, the phy treatment was able to modulate the cardiovascular responses promoting a significant increase of SAP, followed by reflex bradycardia in SHR and Wistar rats. These responses were more intense in Wistar rats. There was no significant difference for Ttail and Tint in the SHR group, however, phy positively impacted the physical performance. Taken together, these results provide evidence that at rest the central cholinergic stimulation modulates thermoregulatory responses through changes in the cardiovascular system of Wistar and SHR rats, and SHR rats presented greater cardiovascular and thermoregulatory responses than normotensive rats after central cholinergic stimulation. During physical exercise the central administration of phy promotes adjustments in the cardiovascular system of normotensive and hypertensive rats. Although these adjustments were not sufficient to pair the thermoregulatory responses in SHR rats, they had a positive impact on physical performance.

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Freercks, Robert Jeremy. « The impact of vascular calcification on ambulatory and central aortic blood pressure in a South African dwelling dialysis population : a clinical, radiological and pathophysiological study of vascular health in a young prevalent dialysis population in a developing country ». Master's thesis, University of Cape Town, 2011. http://hdl.handle.net/11427/11995.

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Includes abstract.
Includes bibliographical references.
In Sub-Saharan Africa, the prevalence of vascular calcification (VC) in CKD-5D is unknown. We undertook to determine the effect of ethnicity on VC, the risk factors for VC, the utility of abdominal X-ray (AXR) in predicting coronary calcium score (CCS) and the effect of VC on central aortic systolic pressure (CASP) and left ventricular mass index (LVMI) in South African dialysis patients. ... Black race significantly protects from VC in South African CKD-5D patients and warrants further study. The AXR is a useful screening tool for CCS in our population. VC does not appear to influence CASP in our population.

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Noel-Morgan, Jessica. « Comparação da reposição volêmica aguda guiada por variação de pressão de pulso e por metas convencionais de ressuscitação em modelo suíno de choque hemorrágico com endotoxemia ». Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5152/tde-09052016-142243/.

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Introdução: A fluidoterapia é o tratamento de primeira linha para pacientes em choque hemorrágico ou choque séptico para restauração do volume circulante e da perfusão tecidual, mas diversas questões relacionadas a este tópico permanecem em debate, particularmente em relação às metas de ressuscitação representadas por variáveis fisiológicas a serem atingidas. A variação de pressão de pulso (VPP) já foi proposta como índice confiável para predição de fluido-responsividade em pacientes sob ventilação mecânica, mas requer avaliação complementar em variadas condições fisiopatológicas. Objetivo: O propósito do presente estudo foi comparar, em um modelo experimental de choque hemorrágico agudo com endotoxemia, uma estratégia de ressuscitação volêmica aguda guiada por VPP e pressão arterial média (PAM) a outra baseada em metas de ressuscitação convencionalmente empregadas envolvendo pressão venosa central (PVC), PAM e saturação venosa mista de oxigênio (SvO2). O modelo experimental foi desenvolvido para esta finalidade e cada variável empregada como meta foi adicionalmente avaliada quanto à capacidade de predição de fluido-responsividade. Métodos: Cinquenta e um porcos foram anestesiados, mecanicamente ventilados e, após preparo, aleatoriamente divididos em seis grupos: controle (Sham, n=8); infusão intravenosa de endotoxina em doses decrescentes (LPS, n=8); choque hemorrágico obtido por meio da retirada de 50% da volemia estimada em 20 minutos (Hemo, n=8); choque hemorrágico com endotoxemia conforme protocolos dos grupos LPS e Hemo (Hemo+LPS, n=9); choque hemorrágico com endotoxemia e, após 60 minutos, ressuscitação com cristalóides para atingir metas: PVC 12-15 mmHg, PAM ≥ 65 mmHg e SvO2 ≥ 65% (Conv, n=9); choque hemorrágico com endotoxemia e, após 60 minutos, ressuscitação com cristalóides para atingir as metas VPP ≤ 13% e PAM ≥ 65 mmHg (dPP, n=9). Tratamentos foram realizados por três horas. Além da avaliação hemodinâmica incluindo termodiluição e ecocardiografia transesofágica, foram realizadas gasometria arterial com mensuração de eletrólitos e lactato, gasometria venosa mista e tonometria intestinal. Ventilação regional foi avaliada por tomografia por impedância elétrica. Mensuração de citocinas séricas e exames histopatológicos pulmonares também foram efetuados. Resultados: Todos os animais dos quatro grupos que receberam a endotoxina desenvolveram hipertensão pulmonar e lesão pulmonar aguda ao longo do experimento. O grupo Hemo+LPS apresentou alta mortalidade (56%), com alterações hemodinâmicas mais acentuadas do que as observadas nos grupos Hemo e LPS. Os grupos Conv e dPP apresentaram o mesmo grau de comprometimento hemodinâmico observado inicialmente no grupo Hemo+LPS, mas houve rápida recuperação em reposta ao tratamento e todos sobreviveram. Entre os grupos tratados não houve diferenças significantes em relação ao volume de cristalóides administrado (volume total, P=0,066) ou ao débito urinário, mas a PVC no grupo Conv foi significantemente superior à dos grupos dPP (P=0,031) e Sham (P=0,048) ao final do protocolo. Entre as variáveis utilizadas como metas, áreas sob as curvas de características operacionais para predição de fluido-responsividade foram maiores para PVC (0,77; IC95%, 0,68-0,86) e VPP (0,74; IC95%, 0,65-0,83), sendo ambas estas variáveis selecionadas por regressão logística múltipla como variáveis independentes para predição de não-responsividade ao desafio volêmico (PVC: P=0,001, razão de chances, 1,7; IC95%, 1,25-2,32 e VPP: P=0,01, razão de chances, 0,91; IC95%, 0,84-0,98). O melhor valor de corte para VPP para maximização de sua função preditiva foi 15%, com sensibilidade 0,75 (IC95%, 0,63-0,85) e especificidade 0,64 (IC95% 0,49-0,77%). Resultados falso-positivos para VPP foram observados em condições de pressão arterial pulmonar média ≥ 27 mmHg e gradiente transpulmonar ≥ 14 mmHg, acompanhados de índice de resistência vascular pulmonar médio > 3 unidades Wood. Resultados falso-negativos também foram constatados. Conclusões: O presente modelo experimental de choque hemorrágico agudo com endotoxemia produziu intenso comprometimento hemodinâmico, hipertensão pulmonar, lesão pulmonar aguda e, na ausência de tratamento, alta mortalidade. Nestas condições, a ressuscitação aguda com cristalóides guiada por VPP e PAM não produziu resultados inferiores à estratégia guiada por metas de ressuscitação convencionalmente estabelecidas, com base em PVC, PAM e SvO2. A principal diferença em desfecho entre as estratégias de ressuscitação foi indução de uma PVC significantemente maior no segundo grupo, ao final do protocolo. Apesar de seus desempenhos individuais terem sido considerados limitados em relação à predição de fluido-responsividade, PVC e VPP foram preditoras independentes de não-responsividade ao desafio volêmico, de modo que sua aplicação em conjunto deva ser investigada. VPP é proposta como uma variável adicional para auxiliar no monitoramento de pacientes, sendo o conhecimento de suas limitações indispensável.
Introduction: Fluid therapy is first-line treatment for patients in hemorrhagic or septic shock for the restoration of circulating volume and tissue perfusion, but several issues remain under debate, particularly regarding resuscitation goals represented by physiological variables to be achieved. Pulse pressure variation (PPV) has been proposed as a reliable index for the prediction of fluid responsiveness in mechanically ventilated patients, but further evaluation for its use in diverse conditions is required. Objective: To compare acute fluid resuscitation guided by PPV and mean arterial pressure (MAP) to another strategy consisting of conventionally-established goals, based on central venous pressure (CVP), MAP and mixed-venous oxygen saturation (SvO2), during experimental acute hemorrhagic shock with endotoxemia. An experimental model was developed to this end and each variable used as resuscitation goal was evaluated additionally for its ability to predict fluid-responsiveness. Methods: Fifty-one pigs were anesthetized, mechanically ventilated and, after preparation, randomized into six groups: control (Sham, n=8); intravenous infusion of endotoxin in decreasing doses (LPS, n=8); hemorrhagic shock of 50% the estimated blood volume in 20 minutes (Hemo, n=8); hemorrhagic shock with endotoxemia in accordance with protocols in groups LPS and Hemo (Hemo+LPS, n=9); hemorrhagic shock with endotoxemia followed by resuscitation with crystalloids, after 60 minutes, to achieve and maintain CVP 12-15 mmHg, MAP ≥ 65 mmHg and SvO2 ≥ 65% (Conv, n=9); hemorrhagic shock with endotoxemia followed by resuscitation with crystalloids, after 60 minutes, to achieve and maintain PPV ≤ 13% and MAP ≥ 65 mmHg (dPP, n=9). Treatments lasted for three hours. In addition to hemodynamic assessment including thermodilution and transesophageal echocardiography, arterial blood-gases with measurement of electrolytes and lactate, mixed-venous blood-gases and intestinal tonometry were performed. Regional ventilation was evaluated by electrical impedance tomography. Lung histopathology and measurement of serum cytokines were performed as well. Results: All animals from the four groups submitted to endotoxemia developed pulmonary hypertension and acute lung injury over the experimental period. Group Hemo+LPS presented with a high mortality rate (56%) and hemodynamic impairment which was more intense than that observed in groups Hemo or LPS. Groups Conv and dPP developed the same degree of hemodynamic compromise observed in group Hemo+LPS initially, but there was quick recovery in response to treatment and all pigs survived. Between treated groups there were no significant differences in amounts of crystalloids infused (total volume, P=0.066) or in urinary output, but CVP in group Conv was significantly higher than in groups dPP (P=0.031) and Sham (P=0.048) at the end of the study period. Among variables used as goals, areas under the receiver-operator characteristic curves regarding prediction of fluid-responsiveness were larger for CVP (0.77; 95%CI, 0.68-0.86) and PPV (0.74; 95%CI, 0.65-0.83), and both these variables were selected by multiple logistic regression as independent predictors of non-responsiveness to fluid challenge (CVP: P=0.001, odds ratio, 1.7; 95%CI, 1.25-2.32 and PPV: P=0.010, odds ratio, 0.91; 95%CI, 0.84-0.98). Best cutoff value to maximize the predictive function of PPV was 15%, with sensitivity 0.75 (95%CI, 0.63-0.85) and specificity 0.64 (95%CI 0.49-0.77). False positive results for PPV were observed at mean arterial pressure ≥ 27 mmHg and transpulmonary gradient ≥ 14 mmHg, with mean pulmonary vascular resistance index > 3 Wood units. False negative results were also detected. Conclusions: This model of acute hemorrhagic shock with endotoxemia produced severe hemodynamic compromise, pulmonary hypertension, acute lung injury and, in the absence of treatment, a high mortality rate. In this setting, acute resuscitation with crystalloids guided by PPV and MAP was not inferior to the strategy guided by conventionally-established goals, based on CVP, MAP and SvO2. The main difference in outcome between resuscitation strategies was the induction of a significantly higher CVP in the second group, at the end of protocol. Although their individual performances were considered limited for the prediction of fluid-responsiveness, CVP and PPV were independent predictors of non-responsiveness to fluid challenge, so that their combined use should be investigated further. PPV is proposed as an additional variable to aid in patient monitoring, but awareness of its limitations is indispensable.

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Quagliotto, Edson. « Efeito da microinjeção de neurotransmissores e neuropeptídeos no núcleo póstero-dorsal da amígdala medial no controle cardiovascular em ratos ». reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2011. http://hdl.handle.net/10183/55618.

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O subnúcleo póstero-dorsal da amígdala medial (AMePD) de ratos modula comportamentos sociais, como é o reprodutivo, e respostas a estímulos estressantes. Para tanto, são necessários ajustes concomitantes da função cardiovascular. Dada sua notável presença no AMePD, o glutamato (GLU), o ácido δ-aminobutírico (GABA), a ocitocina (OT), a somatostatina (SST) e a angiotensina II (Ang II) poderiam estar envolvidos em tais ajustes homeostáticos. O objetivo deste trabalho foi avaliar o efeito da microinjeção de GLU, GABA, OT, SST e Ang II microinjetados diretamente no AMePD de ratos não anestesiados sobre o controle cardiovascular em situação basal e após estimulação dos barorreceptores e quimiorreceptores. Ratos machos Wistar (3 meses de idade) foram mantidos em condições padrão de biotério e cuidados éticos. Os animais foram anestesiados e submetidos à cirurgia estereotáxica para implantação unilateral de cânula no AMePD, lado direito. No quinto dia pós-cirúrgico, os animais foram novamente anestesiados e submetidos à colocação de cateter de polietileno na luz da artéria aorta abdominal e outro na veia cava inferior. Um dia após a canulação dos vasos, os animais foram microinjetados no AMePD com solução salina (0,3 μl; n = 8), GLU na dose de 2 μg/0,3 μl (n = 7), GABA nas doses de 61 ng/0.3μl (n = 7) e de 100 μg/0.3 μl (n = 7), OT nas doses de 10 ng/0,3 μl (n = 7) e de 25 pg/0,3 μl (n = 6), SST nas doses de 1 μM/0,3μl (n = 8) e de 15 fmol/0,3μl (n = 5) e Ang II nas doses de 50 fmol/0,3 μl (n = 7) e de 50 pmol/0,3 μl (n = 7). Dados de frequência cardíaca (FC) e de pressão arterial (PA) foram registrados por 15 minutos em período basal, controle, e, a seguir, foram microinjetadas as substâncias mencionadas e testadas as variáveis de interesse. Os reflexos pressóricos foram testados pela injeção de fenilefrina (8 μg/ml) e nitroprussiato de sódio (100 μg/ml) e os quimiorreceptores, pela de cianeto de potássio (doses crescentes desde 60 até 180 μg/kg). O modelo autoregressivo de análise espectral e a análise simbólica foram utilizados para avaliar a variabilidade da FC e da PA e as atividades simpática e vagal responsáveis pela variabilidade nos dados registrados. Os dados foram comparados pelo teste da análise da variância (ANOVA) de duas vias para medidas repetidas e pelo teste post hoc de Newman- Keuls ou pela ANOVA de uma via e pelo teste de Tukey, conforme apropriado. O nível de significância estatística foi estabelecido em p < 0,05. Não houve diferença estatística entre os grupos estudados nos valores de FC, PA sistólica, PA diastólica e PA média em situação basal ou após as diferentes microinjeções nos grupos microinjetados com neurotransmissores ou com os neuropeptídeos estudados (p > 0,05). Microinjeções de salina, de GLU (2 μg) ou GABA (61 ng ou 100 μg; n = 7 cada grupo) não afetaram os parâmetros basais ou respostas do quimiorreflexo. Os valores correspondentes à curva da modificação da PAM de acordo com a variação da FC foram estatisticamente diferentes entre os grupos estudados, sendo que a curva após a microinjeção de GABA 61 ng no AMePD foi diferente dos grupos que receberam salina ou GABA na maior dose (100 μg; p < 0,05 em ambos os casos). No que se refere ao platô de taquicardia, a curva de inclinação dos dados referente à sensibilidade média do barorreflexo foi diferente entre os grupos que receberam GLU ou GABA em ambas as doses em comparação com o que recebeu salina (p < 0,01). O GLU aumentou valores índices das análises espectral e simbólica simpáticos relacionados com modulações cardíaca e vascular (P <0,05). A administração de GABA (61 ng) também induziu os maiores valores de variabilidade na FC (P <0,05) que pode ser e associado a uma ativação parassimpática central. No grupo de animais microinjetados com salina, OT (10 ng e 25 pg), SST (1μM e 15 fmol) e Ang II (50 fmol e 50 pmol) no AMePD, os valores mais próximos do basal foram obtidos com a menor dose de KCN (60 μg/kg) e ocorreu, conforme o esperado, uma redução estatisticamente significativa maior na FC quando foram aumentadas as doses injetadas de KCN para 100 μg/kg, 140 μg/kg ou 180 μg/kg (teste de Newman-Keuls, p < 0,001 em todos os casos, quando comparadas com a menor dose injetada). Ang II na dose de 50 pmol microinjetada no AMePD gerou maior diminuição reflexa na FC quando comparado com o grupo controle após a estimulação dos quimiorreceptores com KCN nas doses de 60 e 140 μg/kg (p < 0,05). Ang II na dose de 50 pmol microinjetada no AMePD gerou maior diminuição reflexa na PA quando comparado com o grupo controle após a estimulação dos quimiorreceptores com KCN na dose de 140 μg/kg (p < 0,05). Os valores referentes ao ponto de maior inclinação da curva pressórica referente a respostas geradas pelos barorreceptores, (PA50), após injeções de fenilefrina e nitroprussiato de sódio, foram menores nos ratos que receberam OT na dose de 10 ng ou SST na dose de 1 μM microinjetadas no AMePD, quando comparado ao grupo controle (p < 0,05). Os valores referentes à sensibilidade média do barorreflexo (ganho em bpm/mmHg), após injeções de fenilefrina e nitroprussiato de sódio, foi maior no grupo que recebeu OT na dose de 10 ng quando comparado com a Ang II na dose de 50 pmol. Houve maior variabilidade na PA sistólica, na FC, no componente de baixa e de alta frequência do tacograma e no índice de atividade simpático-vagal da análise espectral nos grupos que receberam OT nas doses de (10 ng e 25 pg), SST (1μM e 15 fmol) e Ang II na dose de 50 pmol (p < 0,05). Tais dados, indicam que o AMePD se vale de sua atividade glutamatérgica, GABAérgica, ocitocinérgica, somatostatinérgica e angiotensinérgica local, por circuitaria própria ou devido a aferências neurais, para modificar variáveis cardiovasculares provavelmente concomitantemente à organização de comportamentos.
The postero-dorsal subnucleus of the medial amygdala (MePD) modulates social behavior of rats, such as reproduction, and responses to stressful stimuli. To this end, concomitants adjustments of the cardiovascular function are modulate. Given its remarkable presence in the MePD, glutamate (GLU), Gamma-amino butyric acid (GABA), oxytocin (OT), somatostatin (SST) and angiotensin II (Ang II) could be involved in such homeostatic adjustments. The objective of this study was to evaluate the effect of microinjection of GLU, GABA, OT, SST and Ang II microinjected directly into the rats MePD on non-anesthetized of cardiovascular control under basal conditions and after stimulation of baroreceptors and chemoreceptors. Male Wistar rats (3 months old) were maintained under standard laboratory conditions and ethical care. The animals were anesthetized and submitted to unilateral stereotactic surgery for implantation of the cannula in the right MePD. On the fifth postoperative day, the animals were again anesthetized and underwent placement of polyethylene catheter in the abdominal aorta and inferior vena cava. One day after the cannulation of the vessels, the animals were microinjected with saline solution, GLU (2 μg/0,3 μl, n = 7), GABA (61 ng/0.3μl, n = 7 and 100 μg/0.3 μl, n = 7), OT (10 ng/0,3 μl, n = 7 and 25 pg/0,3 μl, n = 6), SST (1 μM/0,3μl, n = 8 and 15 fmol/0,3μl, n = 5) and Ang II (50 fmol/0,3 μl, n = 7 and 50 pmol/0,3 μl, n = 7) in the MePD. Data for heart rate (HR) and blood pressure (BP) were recorded for 15 minutes at baseline and then were microinjected the substances aforementioned and tested the variables of interest. Baroreceptor function was tested by phenylephrine (8 μg/ml) and sodium nitroprusside (100 μg/ml) injections. Chemoreflex was tested by potassium cyanide (60 – 180 μg/ml) injections. The autoregressive model of symbolic analysis and spectral analysis were used to evaluate the variability of HR and BP and the sympathetic and vagal activities responsible for variability in the data recorded. The data were compared by a two-way analysis of variance (ANOVA) test for repeated measures and the post hoc Newman-Keuls or an one-way analysis of variance (ANOVA) test for repeated measures and the post hoc Newman-Keuls whenever appropriate. The level of statistical significance was set at P ≤ 0.05. There was no statistical difference between groups in the values of HR, systolic BP, diastolic BP and mean BP at baseline or after microinjections in the different groups (P > 0.05). Microinjections of saline, GLU (2 μg) or GABA (61 ng or 100 μg; n = 7 each group) did not affect the basal or responses the of chemoreflex. The values of the curve of change in the MAP in accordive to the variation of HR, were statistically different between groups, and the curve after the microinjection of GABA 61 ng in the MePD was different in the groups that received saline or the highest GABA dose (100 μg, P < 0.05 in both cases). With regard to the plateau of tachycardia, the slope of the data on the average baroreflex sensitivity was different among the groups receiving GLU or GABA at both doses compared to that received saline (P < 0.01). GLU increased power spectral and symbolic sympathetic indexes related with both cardiac and vascular modulations (P < 0.05). The GABA administration (61 ng, but not 100 μg) also induced higher values of HR variability (P < 0.05), rather associated with a parasympathetic activation. In the group of animals microinjected with saline, OT (10 ng and 25 pg), SST (1μM and 15 fmol) and Ang II (50 fmol and 50 pmol) in MePD, there was as expected, a statistically significant greater reduction in HR increasing when the injected doses of KCN to 100 μg/kg, 140 μg/kg or 180 μg/kg (Newman-Keuls test, P < 0.001 in all cases when compared with the lower injected dose). Ang II at the dose of 50 pmol generated a higher reflex decrease in HR compared to the control group after stimulation of the chemoreceptors with KCN at doses of 60 and 140 μg/kg (P < 0.05). Ang II at the dose of 50 pmol generated a higher reflex decrease in BP compared with the control group after stimulation of the chemoreceptors with KCN at the dose of 140 μg/kg (P < 0.05). The values for the point of greatest slope of the AP response generated by baroreceptors (MAP50) was lower in rats given OT at the dose of 10 ng or SST at the dose of 1 μM compared to the control group (P < 0.05). The average values for the baroreflex sensitivity (gain in bpm/mm Hg) after the injection of phenylephrine and sodium nitroprusside was greater in the group receiving OT at the dose of 10 ng compared with Ang II at the dose of 50 pmol. There was a greater variability in systolic BP, HR, the component of low and high frequency of tachogram and the sympathovagal index studied by spectral analysis in the groups that received OT (10 ng and 25 pg), SST (1 μM and 15 fmol) and Ang II (50 pmol; P < 0.05). These data indicate that the MePD has a glutamatergic, GABAergic, ocitocinergic, somatostatinergic angiotensinergic modulatory activity on cardiovascular response most likely involved in the central organization of behaviors.

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Černiauskaitė, Ina. « Slaugytojo vaidmuo prižiūrint centrinius venos kateterius reanimacijos ir intensyvios terapijos skyriuje ». Master's thesis, Lithuanian Academic Libraries Network (LABT), 2014. http://vddb.library.lt/obj/LT-eLABa-0001:E.02~2009~D_20140626_192344-28544.

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Darbo tikslas. Ištirti slaugytojo vaidmenį prižiūrint centrinių venos kateterius reanimacijos ir intensyvios terapijos skyriuje. Darbo uždaviniai. Nustatyti centrinės venos kateterizacijos įtaką pagrindiniams pacientų gyvybinių funkcijų rodikliams. Ištirti, kokios dažniausiai pasitaiko centrinių venų komplikacijos ir jų priežastis. Išsiaiškinti slaugytojo veiksmus, padedančius sumažinti komplikacijų atsiradimo riziką. Ištirti reanimacijos ir intensyvios terapijos slaugytojų centrinių venų kateterių priežiūros žinias . Tyrimo medžiaga ir metodai. Teorinė mokslinės literatūros, leidinių, publikacijų apžvalga. Dokumentų analizės metodas (panaudotas pacientų su centrinių venų kateteriais tyrimui). Asmeninio stebėjimo metodas. Atliktas 97 pacientų po centrinių venų kateterizacijų, pagrindinių gyvybinių funkcijų stebėjimas reanimacijos ir intensyvios terapijos skyriuje. Reanimacijos ir intensyvios terapijos slaugytojų anketinė apklausa žinioms ištirti, dirbant su centrinių venų kateteriais. Gautų rezultatų aptarimas ir jų analizė. Statistinė analizė atlikta naudojant „Microsoft Office Excel 2003“ ir SPSS 16,0 for Windows versijos statistinę programą Tyrimo rezultatai ir išvados. Tam, kad būtų išsiaiškintas slaugytojos vaidmuo prižiūrint centrinius venos kateterius buvo atliktas stebėjimo tyrimas pacientų po centrinių venos kateterizacijų. Tyrimo metu Vilniaus Universiteto ligoninėje Santariškių klinikos I reanimacijos ir intensyvios terapijos skyriuje nustatyta, kad centrinių venos... [toliau žr. visą tekstą]
The goal of the study: to determine the role of a nurse in the maintenance of the central venous catheter (CVC) in the resuscitation and intensive care department. The objectives: to determine the influence of the central venous catheterization to the indexes of the main vital functions of the patients. To specify the most frequent venous complications and the reasons why they occur. To find out what nurses’ actions can reduce the risk of complications. To examine the professional knowledge of the nurses who work with central venous catheters in the resuscitation and intensive care departments. Research material and methods. Theoretical review of scientific literature, publications and articles. Document analysis method (utilized for the reasearch of patient’s with central venous catheters). Personal observation method. Observation of the main vital functions of 97 patients after central venous catheterization in the resuscitation and intensive care department. The questionnaire-based survey in order to examine the professional knowledge of the nurses who work with central venous catheters in the resuscitation and intensive care department. Discussion and analysis of the obtained results. Analysis of the statistical data using the Microsoft Office Excel 2003 and SPSS 16,0 for Windows software packages. The results and conclusions of the study. In order to determine the role of a nurse for the maintenance of central venous catheter, the observation research was conducted with... [to full text]

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Miersch, André. « Außentemperatur, Jahreszeit und individuelle Trajektorien beeinflussen den Blutdruck von Kindern, Jugendlichen und jungen Erwachsenen ». Doctoral thesis, Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-143309.

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Background: Seasonal fluctuations in outdoor temperature have been shown to affect blood pressure in adults. We have asked whether or not there is either a seasonal variation or an influence of outdoor temperature on blood pressure measurements in children and adolescents in middle Europe. Methods: Blood pressure was routinely measured in healthy and sick children and adolescents in outpatient clinics and during hospitalisation in a total of 6714 subjects (3,497 boys/3,237 girls), age 3 to 21 years, with a median of 10.6 years. Results: Cross-sectional analysis showed a significant seasonal variation in blood pressure measurements. The mean increase of systolic and diastolic blood pressure was 4.45/2.42 mmHg during winter. A significant correlation between average outdoor temperatures and systolic blood pressure was found (ρ=-0.074 p<0.001). However, the effect was only detectable at an average temperature below 0° C/32° F and above 10° C/50° F. For each degree Celsius increase in average outdoor temperature, the systolic blood pressure fell by 0.12 mmHg. Conclusion: Blood pressure measurements in children and adolescents, even in a temperate climate, are influenced by temperature and seasonal variation. Considering seasonal variations in blood pressure could be of clinical interest
Background: High blood pressure is a major risk factor for cardiovascular disease. Blood pressure tracking could help to identify individuals with potential hypertension. Therefore, we have asked whether or not tracking was of predictive value for the development of hypertension in early life. Methods: Blood pressure was routinely measured in 13,261children and adolescents in outpatient clinics as well as during hospitalization. In a sub-analysis 568 individuals with normotensive and elevated blood pressure were compared after three follow-up periods (two, four and six years) and 2,157 normotensive individuals were compared in a paired t-test. Results: The follow-up analysis showed a significant tracking effect. However, the Pearson correlation coefficients of the systolic and diastolic blood pressure SDS decreased over time. Upon the follow-up after six years 35.6% of the children and adolescents with elevated blood pressure values remained in the elevated range group. Of the children within the normotensive blood pressure range 80.4% remained normotensive after six years. Children with normotensive blood pressure showed a stronger tracking than those who had had one hypertensive blood pressure reading. Children with high body weight gain left their SDS track to higher blood pressure values. Conclusion: Blood pressure tracking in children and adolescents is moderate. We conclude that the predictive power of a single hypertensive blood pressure measurement during a single visit is rather small, and thus repetitive measurements across several consecutive visits are necessary

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Rezailashkajani, Mohammadreza. « Cardiovascular risk in ageing men of different ethnicities : inter-relationships between imaging and endocrine markers ». Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/cardiovascular-risk-in-ageing-men-of-different-ethnicities-interrelationships-between-imaging-and-endocrine-markers(504c0fa3-280e-4206-94b6-e6093fb5e87b).html.

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Cardiovascular disease varies by ethnicity in the UK. South Asians (SA) have higher coronary heart disease (CHD) and diabetes prevalence, while African-Caribbeans (AfC) have greater stroke, but intriguingly lower CHD rates despite higher blood pressures and diabetes risk than Europeans. Conventional risk factors do not fully explain such differences. This cross-sectional study tested the hypothesis that the hormones, vitamin D measured as 25(OH)D and aldosterone, would be independently associated with intermediate cardiovascular outcome markers in these ethnic groups. Community-dwelling men 40-80 years old (AfC: n=67, 55±10yr; SA: n=68, 55±10yr; European: n=63, 57±8yr) were sampled from Greater Manchester’s multi-ethnic population. The intermediate markers examined were aortic pulse wave velocity (aPWV), left ventricular (LV) mass and function, and carotid intima media thickness (CIMT), measured non-invasively by ultrasound, and hemodynamic profiling methods (the Arteriograph) in the total sample and by magnetic resonance imaging (MRI) in a subsample of 50. Adjusted for age, systolic blood pressure and diabetes, mean(SE) aPWV by the Arteriograph, was 0.5(0.2) m/s higher in SA than AfC and Europeans (p=0.01), which paralleled known cross-ethnic CHD risk differences in the UK. By MRI, aPWV along the descending aorta in SA was 0.7(0.3) and 0.8(0.3) m/s higher than that in AfC and Europeans, but aPWV along the aortic arch was not significantly different. Unlike aldosterone, 25(OH)D was independently and inversely correlated with aPWV (unstandardised B(SE)=-0.013[0.004] m/s, p<0.001), and partly explained the ethnic variation in aPWV. Similar inverse correlations were found between 25(OH)D and LV concentricity measured by echocardiography and MRI. Compared to Europeans, SA and AfC, had 21(3) and 14(3) nmol/L lower mean(SE) 25(OH)D, respectively (p<0.01). Mean(SE) of relative wall thickness, an index of LV concentricity by echocardiography, was 0.05(0.01) higher in SA and AfC than Europeans. Lower 25(OH)D levels were also associated with higher myocardial deformation rates measured by MRI myocardial tagging (n=50), supporting previous animal experimental evidence. A one standard deviation (SD) decrease in 25(OH)D was associated with a 0.38 SD increase in absolute systolic strain rate (p=0.003) and 0.22 SD rise in diastolic strain rate (p=0.04). Right and left CIMT showed different relations with 25(OH)D and aldosterone. Left-right CIMT differences varied by ethnicity and were related to SA ethnicity and aldosterone levels. Two related technical studies investigated the relatively new method of hemodynamic profiling, the Arteriograph, used here. The results suggested a standardisation method of aortic length estimation for purely central aPWV, which significantly improved aPWV agreement between the Arteriograph and MRI (reference method here), and was used for calibrating the Arteriograph aPWV in the above-mentioned results for the total sample. Future well-designed trials are necessary to investigate any cause-effect relationship between vitamin D deficiency and the unfavourable cardiovascular intermediate outcomes found here in a cross-sectional design and multi-ethnic background.

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Anske, Ute. « Chronopsychobiologische Pilotstudie zur objektiven Bestimmung funktioneller Gesundheitszustände ». Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2003. http://dx.doi.org/10.18452/14965.

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1. Unterschiedliche Definitionen der Gesundheit mit verschiedenen Betrachtungsweisen (WHO: Der Mensch eine biopsychosoziale Einheit. Schulmedizin: ohne klinischen und paraklinischen Befund mit Orientierung an kritikbedürftigen Referenzmittelwerten) führt bei Fachleuten, Behörden und Laien zu Verwirrungen, wenn es um die Beurteilung gesundheitlicher Schäden geht. 2. Es wurde die Aufgabe gestellt zu prüfen, welche der beiden Definitionen der Realität näher kommt. 3. Mittels der chronopsychobiologischen Regulationsdiagnostik, des Dreiphasenentspannungstests (Hecht und Balzer 2001), wurden unter dem Aspekt der beiden Gesundheitsdefinitionen drei Gruppen untersucht (je 40 Probanden). - klinisch Gesunde (klinisch Gesunde nach Schulmedizin ) - Gesunde nach Definition der WHO - Probanden mit nichtorganische Insomnie (ohne pathologische klinische und paraklinische Befunde) 4. Die mit den verwendeten Methoden gewonnenen Daten wiesen aus, dass zwischen den klinisch Gesunden und den Probanden mit nichtorganischer Insomnie weitgehend größere Ähnlichkeiten bestehen. Beide Gruppen zeigten aber zu der Gruppe der Gesunden nach WHO-Definition, welche die biopsychosoziale Einheit des Menschen berücksichtigt, noch hochsignifikante Unterschiede. Die Gruppe der klinisch Gesunden kann daher auf Grund unserer Ergebnisse nicht den Anspruch erheben, real gesund zu sein. 5. Mit der Bezugnahme auf die Internationale Klassifikation der Krankheiten (ICD 10F) haben die von uns untersuchten klinisch Gesunden und die nichtorganischen Insomniker eine mehr oder weniger stark ausgeprägte Symptomatik von psychischen Störungen. Dies müsste bei der Beurteilung von Schadstoff-, Lärm-, und EMF-Wirkungen auf den Menschen, wie auch bei den klinisch-pharmakoloischen Untersuchungen beachtet werden. Die in der Arbeit erzielten Ergebnisse bedürfen durch weitere Untersuchungen eine Fundierung. Sie signalisieren aber sowohl unter praktischen als auch unter theoretischen Aspekten einen dringenden Forschungsbedarf.
1. Differing definitions of health using different criterea (WHO: The human being as a bio- psycho-social unit versus classical medicine: without clinical and paraclinical results based on suspect reference values) bring confusion to experts, authorities and laymen when assessing health damages. 2. The given task was to check which of the two definitions is closer to reality. 3. Using the chrono-psycho-biological diagnostic of regulation, the three-phase-relaxation test (Hecht and Balzer 2001), three groups were examined considering the aspects of the two health definitions (40 test subjects in the study group). - clinically healthy (clinically healthy per classical medicine definition) - healthy per definition of the WHO - test persons with non organic insomnia (i.e. no pathological or paraclinical findings) 4. The data gained from the employed methods revealed bigger similarities between clinically healthy persons and those with non organic insomnia. Both groups still showed highly significant differences to the group which fulfils the definition of the WHO regarding a human as a bio-psycho-social unit. As a result of this study, persons, though classified as "clinically healthy" might nevertheless not absolutely be healthy in reality. 5. In reference to the international classification of illnesses (ICD 10 F) the groups examined, both of clinically healthy and those with non organic insomnia, have more or less severe psychological symptoms. This should be taken into account when assessing the effects of pollution, noise, and EMF as well as clinical pharmacological studies. These present findings still need broader confirmation by further investigations. However, they clearly indicate, for practical and theoretical considerations, an urgent need for further research.

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Finau, Emily. « Transparency and learning spaces ». Thesis, Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/39593.

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This thesis explores the various meanings and implications of transparency in architecture and in learning environments in particular. Architectural transparency, achieved through choice of materials and principles of formal composition, creates a diversity of relationships and can facilitate visual, conceptual, and functional clarity as well as offering simultaneous perception of different spaces. It offers a range of phenomenological qualities and so provides an opportunity to explore and complicate such dichotomies as translucency and opacity, openness and closure, and public space and private space. While celebrated throughout modern and contemporary architecture, transparency raises issues of privacy and safety even as it breaks down hierarchies and social boundaries. The research-based design of transparency in a school building necessitates careful planning to achieve a balance between the access to views, natural light, fresh air, and social interaction that transparency may bring and the continuing obligation to provide a safe, secure environment for schoolchildren.

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Bibiloni, Esteva Maria del Mar. « Estudi de la prevalença de l'obesitat juvenil a les illes Balears ». Doctoral thesis, Universitat de les Illes Balears, 2012. http://hdl.handle.net/10803/84114.

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Teixeira, Ana Sofia da Cunha. « Ageing affects the balance between central and peripheral mechanisms of cerebrovascular regulation with increasing influence of systolic blood pressure levels ». Master's thesis, 2019. https://hdl.handle.net/10216/119825.

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BACKGROUND: Arterial baroreflex (BR) and cerebral autoregulation (CA) are two major regulatory mechanisms that maintain constant cerebral perfusion. Little is known about the interplay between these mechanisms, particularly when considering the effects of ageing or sex.PURPOSE: We studied the relationship between dynamic CA and BR sensitivity (BRS) in healthy subjects by sex and in different age strata.METHODS: 95 healthy adults (52% female), 20-80 years-old, were recruited. Arterial blood pressure (Finometer), 3-lead electrocardiogram and cerebral blood flow velocity in middle cerebral arteries (transcranial Doppler) were monitored. We assessed CA by transfer function analysis and BRS in frequency and time domain.RESULTS: With increasing age, BRS diminished (ANCOVA R2 = 0.281, p < 0.001) but CA parameters did not change significantly (p > 0.05). Overall, there was an inverse relationship between the efficacy of BRS and CA low-frequency gain [multivariate linear regression β = 0.41 (0.31; 0.61), p < 0.001]. However, this association suffers changes with ageing: in older subjects BRS and CA were not correlated [β = 0.10 (- 0.41; 0.62), p = 0.369]. Instead, decreasing systolic blood pressure correlated with less efficient CA [lower CA low-frequency gain β = - 0.02 (- 0.03; - 0.02), p = 0.003]. Sex did not affect BRS and CA relationship.CONCLUSIONS: Cerebral blood supply is governed by a tuned balance between BR and CA which is lost with age as BRS decreases dramatically. Low systolic blood pressure values might be harmful to older subjects as they might reduce the ability to keep cerebral blood flow tightly controlled.

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Teixeira, Ana Sofia da Cunha. « Ageing affects the balance between central and peripheral mechanisms of cerebrovascular regulation with increasing influence of systolic blood pressure levels ». Dissertação, 2019. https://hdl.handle.net/10216/119825.

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BACKGROUND: Arterial baroreflex (BR) and cerebral autoregulation (CA) are two major regulatory mechanisms that maintain constant cerebral perfusion. Little is known about the interplay between these mechanisms, particularly when considering the effects of ageing or sex.PURPOSE: We studied the relationship between dynamic CA and BR sensitivity (BRS) in healthy subjects by sex and in different age strata.METHODS: 95 healthy adults (52% female), 20-80 years-old, were recruited. Arterial blood pressure (Finometer), 3-lead electrocardiogram and cerebral blood flow velocity in middle cerebral arteries (transcranial Doppler) were monitored. We assessed CA by transfer function analysis and BRS in frequency and time domain.RESULTS: With increasing age, BRS diminished (ANCOVA R2 = 0.281, p < 0.001) but CA parameters did not change significantly (p > 0.05). Overall, there was an inverse relationship between the efficacy of BRS and CA low-frequency gain [multivariate linear regression β = 0.41 (0.31; 0.61), p < 0.001]. However, this association suffers changes with ageing: in older subjects BRS and CA were not correlated [β = 0.10 (- 0.41; 0.62), p = 0.369]. Instead, decreasing systolic blood pressure correlated with less efficient CA [lower CA low-frequency gain β = - 0.02 (- 0.03; - 0.02), p = 0.003]. Sex did not affect BRS and CA relationship.CONCLUSIONS: Cerebral blood supply is governed by a tuned balance between BR and CA which is lost with age as BRS decreases dramatically. Low systolic blood pressure values might be harmful to older subjects as they might reduce the ability to keep cerebral blood flow tightly controlled.

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Magbool, Ahmed. « Blind Estimation of Central Blood Pressure Waveforms from Peripheral Pressure Signals ». Thesis, 2020. http://hdl.handle.net/10754/664203.

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The central aortic blood pressure signal is an important source of information that contains cues about the cardiovascular system condition. Measuring this pulse wave clinically is burdensome as it can be only measured invasively with a catheter. As a result, many mathematical tools have been proposed in the past few decades to reconstruct the aortic pressure signal from the peripheral pressure signals that are usually easier to obtain noninvasively. At the distal level, the blood pressure signal is not directly useful since factors, such as length and stiffness of the arteries, play roles in changing the shape of the pressure signal significantly. In this thesis, multi-channel blind system identification techniques are proposed to estimate the central pressure waveform which vary in their accuracy and complex- ity. First, a simple linear method is applied by approximating the nonlinear arterial system as a linear time-invariant system and applying the cross-relation approach. Next, a more complicated nonlinear Wiener system is proposed to model the nonlinear arterial tree. Along with the channel’s coefficients, the nonlinear functions are estimated using cross-relation and kernel methods. Data-driven machine learning methods are tested to estimate the aortic pressure signals. In many cases, they suffer from underfitting problems. As a remedy, a hybrid machine learning and cross-relation approach is also proposed to add more robustness to the machine learning models. This hybrid approach is implemented by combining the cross-relation with any machine learning method, including deep learning approaches. The various methods are tested using pre-validated virtual databases. The results show that the linear method produces root mean squared errors between 3.40 mmHg and 6.24 mmHg depending on the cross-relation constraint and the equalization tech- nique. On the other hand, the root mean squared errors associated with the nonlinear methods are between 3.76 mmHg and 4.22 mmHg and hence more stable. For the hybrid machine learning and cross-relation approach, applying the cross-relation and the dictionary learning reduce the root mean squared errors up o 67% comparing with the pure machine learning models.

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Armstrong, MK. « Central-to-peripheral artery hemodynamics ». Thesis, 2020. https://eprints.utas.edu.au/34810/1/Armstrong_whole_thesis_ex_pub_mat.pdf.

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High blood pressure (BP) is the leading modifiable risk factor for cardiovascular disease (CVD) and death. However, conventional brachial systolic and diastolic BP provide limited information on the underlying BP waveform and do not encompass all the cardiovascular risk associated with BP. Moreover, evidence suggests central (aortic) BP may be more clinically useful than conventional brachial BP, highlighting the importance of differences in central-to-peripheral vascular properties and arterial hemodynamics in the assessment of BP related risk. Recently, the reservoir-excess pressure model has emerged as a construct for deriving clinically relevant information from the underlying BP waveform and may be useful for assessing differences in central-to-peripheral artery hemodynamics. Nevertheless, there is an under-appreciation of the influence of differences in central-to-peripheral vascular properties on arterial hemodynamics and reservoir-excess pressure parameters. Consideration of the changes in vascular properties and a greater awareness of the hemodynamic variability throughout the arterial tree may facilitate a more accurate assessment of BP and BP related risk. Therefore, the broad aims of this research were to determine the hemodynamic differences between central and peripheral arteries and identify clinically useful parameters derived from arterial BP waveform analysis, with a particular focus on reservoir-excess pressure parameters. Evidence suggests the reservoir-excess pressure model has value for deriving physiological and clinically additive information from the underlying BP waveform. However, more research is needed to better understand the value of this model for the assessment of arterial hemodynamics and BP related cardiovascular risk. The reservoir excess pressure model is still in its relative infancy, and there is yet to be a published article that describes the physiological and clinical evidence relating to parameters derived via this model. This gap in the literature is addressed in chapter 1 as part of an invited review for the Journal of Frontiers in Physiology, where we highlight the need for greater appreciation of differences in central-to-peripheral artery hemodynamics and BP waveform morphology. Study 1 (Chapter 2) sought to determine the usefulness of the ratio of aortic-to-brachial artery stiffness (ab-ratio) for assessing central-to-peripheral artery properties. Previously, the ab-ratio has shown promise as a vascular risk marker independent of the influence of BP, but this has only been examined among individuals with disease. Study 1 found that in patients with disease, including renal disease (n=119), type two diabetes mellitus (n=77), and hypertension (n=140), the ab-ratio was not associated with BP (P >0.11 for all). Conversely, among healthy individuals (n=99), the ab-ratio was associated with BP (β = 0.08, P = 0.003). These findings show that the ab-ratio is inherently related to BP and, thus, has limited potential as a tool for the assessment of vascular properties beyond techniques already available. In study 2 (Chapter 3), central-to-peripheral artery hemodynamics were assessed by examination of the differences in intra-arterial BP between the aortic, brachial, and radial arteries among 180 individuals undergoing coronary angiography. The key finding from this study was that systolic BP, the peak of the BP waveform, was, on average, 5.5 mmHg higher in the radial artery compared to the brachial artery accounting for 43% of the difference in systolic BP between the aorta and radial artery. There was significant between-person variability in the level of systolic BP difference between the brachial and radial arteries. Conversely, on average, there were small non-significant decreases for both diastolic and mean BP between the brachial and radial arteries (-1.1 and -1.6 mmHg, respectively). These findings improve our understanding of changes in central-toperipheral artery hemodynamics with implications for novel wrist-based BP devices and estimation of aortic BP via conventional pulse wave analysis methods. Additionally, the consistency of diastolic BP suggests a detailed analysis of diastolic BP waveform morphology via reservoir-excess pressure analysis, may present an opportunity asses central artery hemodynamics from the peripheral artery BP waveform. Study 3 (Chapter 4) sought to determine the uniformity and clinical value of key reservoir-excess pressure parameters derived from central and peripheral artery BP waveforms, with a focus on parameters relating to diastolic BP waveform morphology. Among 220 individuals undergoing a coronary angiography procedure, model parameters were derived from intra-arterial aortic, brachial, and radial BP waveforms, and clinical value was assessed by association with estimated glomerular filtration rate (eGFR). Of all the model parameters, the reservoir pressure and diastolic rate constant were the most uniform between arterial sites. However, only the diastolic rate constant had consistent associations with eGFR when derived from central and peripheral arteries (P <0.03). The diastolic rate constant, therefore, represents a clinically useful marker of BP related risk that, when derived from peripheral arteries, provides clinically important information related to central artery hemodynamics. Finally, study 4 (Chapter 5) examined the relationship of excess pressure to directly measured blood flow velocity. As predominantly a component of systolic BP waveform morphology, excess pressure is modified between central and peripheral arteries. Thus, it was unknown if previous observations of the equivalency of central artery excess pressure to aortic blood flow were applicable in peripheral arteries. Among 97 individuals, intra-arterial BP was recorded via a fluid-filled catheter, and flow velocity was measured via Doppler ultrasonography at the brachial and radial arteries. This study found that in both time and frequency domain analyses, excess pressure derived from brachial and radial arteries was analogous to blood flow velocity, thus affording the opportunity to derive information related to arterial flow using only the BP waveform. These findings are expected to have clinical utility as they may help refine methods for non-invasive hemodynamic monitoring used in the management of the critically ill. In summary, the ab-ratio has limited value as a marker of central-to-peripheral vascular properties as shown in study 1. The second study is the first sufficiently large and robust investigation of central-to-peripheral intra-arterial BP differences, where it was found that the systolic component of BP waveform morphology is, on average, amplified, albeit with major inter-individual variability. Conversely, in study 3 it was discovered that the diastolic rate constant, a parameter derived via the reservoir-excess pressure model related to diastolic waveform morphology, was uniform in both absolute value and association with risk when derived from central and peripheral arteries and may facilitate the assessment of risk related to central artery hemodynamics. Finally, study 4 showed that excess pressure derived from peripheral artery BP waveforms was analogous to flow velocity and may lead to improvements in non-invasive hemodynamic monitoring applicable to the clinical setting. Altogether, this thesis provides a body of new information on central-to-peripheral artery hemodynamics and identifies clinically useful parameters derived from reservoir-excess pressure analysis of the underlying BP waveform. These findings could lead to real-world improvements in the assessment of BP related cardiovascular risk and better BP risk phenotyping.

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