Relevant bibliographies by topics / Cardiovascular regulation

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cardiovascular regulation'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "Cardiovascular regulation"

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Speer, Mei Y., and Cecilia M. Giachelli. "Regulation of cardiovascular calcification." Cardiovascular Pathology 13, no. 2 (March 2004): 63–70. http://dx.doi.org/10.1016/s1054-8807(03)00130-3.

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Versteeg, Dirk H. G., Patricia Van Bergen, Roger A. H. Adan, and Dick J. De Wildt. "Melanocortins and cardiovascular regulation." European Journal of Pharmacology 360, no. 1 (October 1998): 1–14. http://dx.doi.org/10.1016/s0014-2999(98)00615-3.

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WEBB, D. "Endothelin and cardiovascular regulation." American Journal of Hypertension 8, no. 4 (April 1995): 18A. http://dx.doi.org/10.1016/0895-7061(95)97440-3.

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Williamson, Jon W., and William P. Morgan. "Cardiovascular regulation: Spect neuroimaging." International Journal of Sport and Exercise Psychology 3, no. 3 (January 2005): 352–62. http://dx.doi.org/10.1080/1612197x.2005.9671777.

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Trinder, John, Joanna Waloszek, Michael J. Woods, and Amy S. Jordan. "Sleep and cardiovascular regulation." Pflügers Archiv - European Journal of Physiology 463, no. 1 (October 26, 2011): 161–68. http://dx.doi.org/10.1007/s00424-011-1041-3.

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Russell, Fraser. "Urotensin II in cardiovascular regulation." Vascular Health and Risk Management Volume 4 (August 2008): 775–85. http://dx.doi.org/10.2147/vhrm.s1983.

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Sik Park, Kwon, Jang Kyu Choi, and Yang Saeng Park. "Cardiovascular Regulation during Water Immersion." APPLIED HUMAN SCIENCE Journal of Physiological Anthropology 18, no. 6 (1999): 233–41. http://dx.doi.org/10.2114/jpa.18.233.

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da Costa Martins, P. A., S. Leptidis, K. Salic, and L. J. De Windt. "MicroRNA Regulation in Cardiovascular Disease." Current Drug Targets 11, no. 8 (August 1, 2010): 900–906. http://dx.doi.org/10.2174/138945010791591322.

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Laederach-Hofmann, K., L. Mussgay, and H. Ruddel. "Autonomic cardiovascular regulation in obesity." Journal of Endocrinology 164, no. 1 (January 1, 2000): 59–66. http://dx.doi.org/10.1677/joe.0.1640059.

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Obese persons suffer from an increased mortality risk supposedly due to cardiovascular disorders related to either continuously lowered parasympathetic or altered sympathetic activation. Our cross-sectional correlation study establishes the relationship between obesity and autonomic regulation as well as salivary cortisol levels. Three patient cohorts were sampled, covering ranges of body mass index (BMI) of 27-32 (n=17), 33-39 (n=13) and above 40 kg/m(2)(n=12), and stratified for age, sex and menopausal status. Autonomic cardiovascular regulation was assessed by use of heart rate variability and continuous blood pressure recordings. Spectral analytical calculation (discrete Fourier transformation) yields indices of sympathetic and parasympathetic activation and baroreflex sensitivity. Morning salivary cortisol was concurrently collected. Contrary to expectation, BMI and waist/hip ratio (WHR) were inversely correlated with sympathetic activity. This was true for resting conditions (r=-0.48, P<0.001; r=-0.33, P<0.05 for BMI and WHR respectively) and for mental challenge (r=-0.42, P<0.01 for BMI). Resting baroreflex sensitivity was strongly related to the degree of obesity at rest (BMI: r=-0.35, P<0.05) and for mental challenge (r=-0.53, P<0.001). Salivary cortisol correlated significantly with waist circumference (r=-0.34, P=0.05). With increasing weight, no overstimulation was found but a depression in sympathetic and parasympathetic activity together with a significant reduction in baroreflex functioning and in salivary cortisol levels.
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Mingarelli, Maurizio. "The cardiovascular system renal regulation." Nephrology @ Point of Care 2, no. 1 (January 2016): pocj.5000201. http://dx.doi.org/10.5301/pocj.5000201.

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The study of kidney physiology and cardiovascular system physiology has long unveiled several points of contract from which the existence of integrated mechanisms between the two systems has readily been inferred. In conclusion, the need is felt to conduct new studies to explore how the physiologic response to neuro-vegetative stimuli correlates to the renal function level indicated by the glomerular filtration rate (GFR) in a view to demonstrating that a decreased GFR results in cardiovascular alterations whose size is directly proportional to the same GFR reduction.
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Dissertations / Theses on the topic "Cardiovascular regulation"

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O'Neill, Mark. "Cardiovascular regulation under physiological stress." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294358.

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Tur, Jared. "Cardiovascular regulation by Kvβ1.1 subunit." Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6596.

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Heterologous expression systems such as COS-7 cells have demonstrated the profound effects of KCNAB1-3 or Kvβ1-3 proteins on voltage gated potassium channels (Kv) channels. Indeed, in the presence of these β-subunits transiently expressed Kv channels are often modulated in multiple ways. Kv channel membrane expression is often increased in the presence of β-subunits. In addition, non-inactivating Kv currents suddenly become fast-inactivating and fast-inactivating channels become even faster. While much research has demonstrated the profound effects the β-subunits in particular the Kvβ1 subunit have on transiently expressed Kv currents little to date is known of the physiological role it may play. One study demonstrated that by “knocking out” Kvβ1 cardiomyocyte current changes were noted including a decrease in the Ito,f current. While this novel finding demonstrated a key cardiac physiological role of the Kvβ1 subunit it left many unanswered questions as to determine the cardiovascular regulation the Kvβ1 subunit provides. Indeed, cardiac arrhythmias and other electrical abnormalities within the heart such as long QT present patients with many unfortunate unknowns. Many of these incidences occur often abruptly with cardiac electrical abnormalities. Genetic research has begun to shine light on key cardiovascular genes in particular those coding for ion channels and auxiliary subunits or β-subunits. Kv channels and their β-subunits have gained particular notoriety in their key responsibility in restoring the resting membrane potential known as the repolarization phase. Indeed genetic manipulation and physiological examination of Kv channels and recently their β-subunits has demonstrated profound physiological results including prolonged QT durations within mice altered functional activity during physiological cycles such as estrus. While initial findings of Kvβ1 have demonstrated profound cellular and cardiomyocyte current alterations much still remains unknown. Therefore, this work hypothesizes that the Kvβ1 subunit provides a profound cardiovascular role in regulation and redox sensing at the physiological and pathophysiological level in both males and females. This work identifies a sex-based difference in cardiovascular regulation by Kvβ1 as well as demonstrated a profound redox sensing ability during altered metabolic states seen in pathophysiological conditions.
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Ylitalo, A. (Antti). "Cardiovascular autonomic regulation in systemic hypertension." Doctoral thesis, Oulun yliopisto, 1999. http://urn.fi/urn:isbn:9514252128.

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Abstract Neurogenic factors are known to be important in the development of hypertension. Our current knowledge of the role of autonomic nervous system in chronic hypertension is, however, limited. The purpose of the present study was to evaluate the possible abnormalities in heart rate variability (HRV) and baroreflex sensitivity (BRS) in patients with long standing systemic hypertension compared to subjects without evidence of cardiovascular disease. A particular aim was also to examine whether genetic variation in the renin-angiotensin-aldosterone system (RAS) genes have an influence on cardiovascular autonomic regulation. Case-control studies were carried out on a total of 280 normotensive and 214 hypertensive subjects drawn from a random middle-aged population originally recruited for an epidemiologic study of cardiovascular risk factors. The possible association of BRS with the genetic polymorphisms of renin-angiotensin-aldosterone system genes was studied in a cross-sectional study of 315 healthy controls. Genetic associations were also tested in a younger, independent population sample of 66 subjects. The effects of intensified antihypertensive treatment on autonomic cardiovascular control were evaluated in 33 hypertensive patients with poor blood pressure control. Wide interindividual variation in both HRV and BRS was observed in normotensive as well as hypertensive subjects. Overall HRV and autonomic responses to a change in body posture were blunted in long-standing hypertension. Decreased HRV was mainly related to elevated blood pressure and obesity. For the first time in a population-based study, it was confirmed that BRS is impaired in patients with long-standing hypertension despite adequate antihypertensive treatment. In contrast to HRV, BRS was reduced in hypertensive subjects also after adjustment for blood pressure and obesity. BRS also varied widely both between healthy and hypertensive individuals. The wide interindividual variation in the markers of autonomic cardiovascular regulation was not, however, completely explained by demographic variables, cardiovascular risk factors or lifestyle, suggesting a genetic component contributing to HRV and BRS. The polymorphism in the aldosterone synthase (CYP11B2) gene was found to strongly associate with BRS in two independent random populations of apparently healthy subjects. The association was even stronger in the younger population. On the basis of the observations made in the older population, it seems possible that women are protected against the effect of age and blood pressure on BRS and tend to maintain the genomic influence longer. Intensified antihypertensive combination therapy improved blood pressure control and caused regression of left ventricular hypertrophy, and resulted in significant improvements of HRV and BRS. The present study shows that HRV and BRS are altered in long-standing systemic hypertension. Together with age, blood pressure and obesity, genetic factors seem to be important determinants of BRS. However, abnormal autonomic cardiovascular regulation does not seem to be an irreversible phenomenon, but can be partly restored by modern combination antihypertensive therapy.
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Maa, Ming-Hokng 1977. "Alterations in cardiovascular regulation and function assessed using cardiovascular system identification." Thesis, Massachusetts Institute of Technology, 2000. http://hdl.handle.net/1721.1/86525.

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Thesis (S.B. and M.Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2000.
Includes bibliographical references (p. 65-67).
by Ming-Hokng Maa.
S.B.and M.Eng.
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Piira, O. P. (Olli-Pekka). "Effects of emotional excitement on cardiovascular regulation." Doctoral thesis, Oulun yliopisto, 2015. http://urn.fi/urn:isbn:9789526209708.

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Abstract The incidence of adverse cardiovascular events is higher among spectators of exciting sports events, particularly in patients with coronary artery disease (CAD), but the mechanistic link between the events is not known. We assessed the hemodynamic, autonomic function, plasma catecholamines, endothelin-1, interleukin-6, and markers of platelet activation and blood coagulation of enthusiastic male ice hockey spectators with CAD (n=55, 60±9 years) and healthy subjects (n=16, 48±6 years) during Finnish national league ice hockey final play-off matches and on a control day. Blood markers were also measured before and after a maximal exercise test with a bicycle ergometer. Systolic and diastolic blood pressure (BP) were significantly higher one hour before, during, and one hour after the match than on the control day. During the match the highest systolic BP was 180±14 vs. 145±15 and diastolic BP was 103±13 vs. 82±11 mmHg (respectively, p<0.001 for both). Heart rate (HR) was higher throughout the match (p<0.05) and remained elevated two hours after the match (p<0001), and measures of HR variability were decreased during the match (p<0.01). Plasma endothelin-1 (ET-1), interleukin-6 (IL-6) and noradrenaline (NOR) increased during the match (p<0.01 for all), but markers of platelet activation and coagulation remained unchanged. ET-1 did not change during exercise but NOR, adrenaline, IL-6, and markers of platelet activation and blood coagulation increased statistically significantly (p<0.0001 for all). A statistically significantly more marked increase in both endothelin-1 and interleukin-6 was observed in CAD patients compared with healthy subjects during the match (time x group interaction p<0.05 for both). The high-frequency power of R-peak-to-R-peak intervals decreased in CAD patients (p<0.001) but did not change in healthy subjects during the match. Maximal metabolic equivalens (METs) were most strongly correlated with ET-1 response during the match (β =-0.45, partial correlation r=-0.43, p=0.002) when age, body mass index, METs, left ventricular ejection fraction, basal ET-1 and subjective experience of excitement were entered into the model as independent variables in a linear stepwise regression analysis. In conclusion, autonomic reactions and vasoconstriction may partly explain the vulnerability to cardiovascular events caused by this type of leisure-time emotional excitement. Emotional excitement causes concomitant increases in markers reflecting vulnerability to atherosclerotic plaque complications, while physical exercise causes more prominent changes in markers of coagulation. Emotional excitement causes more significant increases of markers of vasoconstriction and acute inflammation and withdrawal of cardiac vagal regulation in patients with CAD than in healthy subjects. Exercise capacity may protect against further cardiovascular events in CAD patients because it is associated with reduced ET-1 release during emotional excitement
Tiivistelmä Jännittävän urheilutapahtuman on havaittu lisäävän sydäntapahtumia erityisesti sepelvaltimotautipotilailla. Syyt eivät ole selvillä. Tutkimuksen kohteena oli jääkiekon mestaruussarjan pudotuspelien seuraamisen vaikutus sekä sepelvaltimotautisten (n=55, 60±9 vuotta) että terveiden (n=16, 48±6 vuotta) jääkiekkofanien verenkiertoon, autonomiseen hermostoon, veren katekolamiinien, endoteliini-1:n (ET-1) ja interleukiini-6:n (IL-6) pitoisuuksiin sekä veren hyytymiseen paikan päällä jäähallissa seurattuna. Muuttujat mitattiin jäähallissa ottelun aikana. Ne mitattiin myös ennen ottelua ja eri päivänä sairaalassa ennen kuntopyörällä tehtyä maksimaalista sydämen kuormitustestiä ja heti sen jälkeen. Sepelvaltimotautipotilaiden ylä- ja alaverenpaineet kohosivat tilastollisesti merkitsevästi tuntia ennen jääkiekkopeliä ja sen aikana, ja ne olivat koholla vielä tunnin ajan pelin jälkeen kontrollipäivään verrattuina. Ottelun aikana yläpaineet olivat 180±14 vs. 145±15 ja alapaineet 103±13 vs. 82±11 mmHg (p<0.001 molemmille painetasoille). Sydämen syke oli korkeampi pelin ajan (p<0.05), ja se pysyi koholla kahden tunnin ajan pelin jälkeen (p<0.001). Lisäksi sykevaihtelu heikentyi pelin aikana (p<0.01) kontrollipäivään verrattuna. Veren ET-1-, IL-6- ja noradrenaliinipitoisuudet (p<0.01) nousivat pelin aikana, mutta veren hyytymistä kuvastavat lukemat säilyivät muuttumattomina. ET-1 ei noussut fyysisessä kuormitustestissä, mutta noradrenaliini- ja adrenaliinipitoisuudet sekä IL-6:n ja veren hyytymistä kuvaavat lukemat kasvoivat tilastollisesti merkitsevästi (p<0.0001). Pelin aikana sepelvaltimotautipotilaiden ET-1 ja IL-6 pitoisuudet kohosivat enemmän kuin terveiden vastaavat arvot (p<0.05). Lisäksi ottelun aikana sydämen sykevaihtelu laski sepelvaltimopotilailla (p<0.001), muttei muuttunut terveillä. Polkupyörätestin maksimaalinen suorituskyky (METs) oli voimakkaasti yhteydessä ET-1 vasteeseen pelin aikana (β =-0.45, r=-0.43, p=0.002), kun ikä, painoindeksi, METs, sydämen supistusvireys, ET-1:n lähtötaso ja koehenkilöiden kokema jännitystaso huomioitiin itsenäisinä muuttujina regressiotyyppisessä tilastolaskennassa. Yhteenvetona todetaan itsenäisesti toimivan hermoston muutosten ja verisuonten supistumisen voivan osittain selittää aiemmin havaitun sydäntapahtumien lisääntymisen tutkimuskohteen tyyppisessä vapaa-ajan tunne-elämyksessä. Jääkiekkopelin jännitys aiheuttaa muutoksia sepelvaltimotautialueiden repeämisherkkyyttä kuvaaviin tekijöihin, kun taas fyysinen rasitus vaikuttaa voimakkaammin veren hyytymistä ilmaiseviin lukemiin. Potilailla jännitys lisäsi enemmän suonten supistuvuutta, akuuttia tulehdusreaktiota ja nosti parasympaattisen hermoston vetäytymistä kuvaavia lukemia terveisiin koehenkilöihin verrattuna. Hyvä suorituskyky voi suojata korkean riskin sepelvaltimotautipotilaita sydäntapahtumilta vähentämällä ET-1:n vapautumista jännityksen aikana
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DeGrande, Sean Thomas. "Phosphatase regulation in cardiovascular physiology and disease." University of Iowa, 2012. http://ir.uiowa.edu/etd/3443.

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Reversible protein phosphorylation is an essential component of metazoan signaling and cardiovascular physiology. Protein kinase activity is required for regulation of cardiac ion channel and membrane receptor function, metabolism, and transcription, and aberrant kinase function is widely observed across disparate cardiac pathologies. In fact, multiple generations of cardiac therapies (eg. beta-adrenergic receptor blockers) have targeted cardiac kinase regulatory cascades. In contrast, essentially nothing is known regarding the mechanisms that regulate cardiac phosphatase activity at baseline or in cardiovascular disease. Protein phosphatase 2A (PP2A) is a key phosphatase with multiple roles in cardiac physiology. Here we demonstrate the surprisingly complex regulatory platforms that control PP2A holoenzyme activity in heart. We present the first full characterization of the expression and regulation of the PP2A family of polypeptides in heart. We identify the expression of seventeen different PP2A genes in human heart and define their differential expression and distribution across species and in different cardiac chambers. We show unique subcellular distributions of PP2A regulatory subunits in myocytes, strongly implicating the regulatory subunit in conferring PP2A target specificity in vivo. We report striking differential regulation of PP2A scaffolding, regulatory, and catalytic subunit expression in multiple models of cardiovascular disease as well as in human heart failure samples. Importantly, we demonstrate that PP2A regulation in disease extends far beyond expression and subcellular location, by identifying and describing differential post-translational modifications of the PP2A holoenzyme in human heart failure. Furthermore, we go to characterize a mechanism for this method of post-translational modification that may represent a pathway capable of being therapeutically manipulated in human heart failure. Lastly we provide evidence that dysregulation of phosphatase activity contributes to the cellular pathology associated with a previously described inheritable human arrhythmia syndrome, highlighting the importance of the PP2A in cardiovascular physiology and disease. Together, our findings provide new insight into the functional complexity of PP2A expression, activity, and regulation in heart and in human cardiovascular disease and identify potentially new and specific gene and subcellular targets for the treatment of human arrhythmia and heart failure.
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Keramatipour, Mohammad. "Regulation of cardiovascular cell phenotype by BTEB3." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616239.

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Way, Monica A. "Regulation of cardiovascular responses from the infralimbic cortex." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq28684.pdf.

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Ferro, Albert. "#beta#-adrenoceptor cross-regulation in the human cardiovascular system." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318286.

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Mcginley, Jared Joseph. "Lateralized Induction of Cardiovascular Responses: Exploring Asymmetric Autonomic Regulation." Thesis, Virginia Tech, 2012. http://hdl.handle.net/10919/32888.

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There is clear evidence that the autonomic nervous system (ANS) is lateralized at both the peripheral as well as the central levels of the nervous system. Both the vagus and the sympathetic ganglia asymmetrically innervate the sino-atrial node and the myocardium of the heart. This lateralization has also been observed in afferent as well as efferent projections to nuclei in the brainstem, hypothalamus, and amygdala. Where laterality has not been as clear is in regions of the frontal lobe dedicated to the regulation of autonomic nervous system responses. This study addressed that issue via the implementation of lateralized autonomic response-evoking tasks. With the use of cardiovascular and electrodermal measures, the present study indexed autonomic responses to lateralized stimuli. This study also explored the role of lateralization within sex as well as in relation to reported gender identity. The findings lend support to the right hemisphere as serving a dominant role in regulating sympathetic nervous system activity, while lending less conclusive support for lateralization of parasympathetic nervous system regulation. Men demonstrated greater lateralization for sympathetic nervous system responses across several different metrics of autonomic indices. The exploration of gender variables in relation to lateralization of autonomic responses was generally not supported.
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Books on the topic "Cardiovascular regulation"

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Dun, Nae J., Benedito H. Machado, and Paul M. Pilowsky, eds. Neural Mechanisms of Cardiovascular Regulation. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9054-9.

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J, Dun Nae, Machado Benedito Honório, and Pilowsky P. M, eds. Neural mechanisms of cardiovascular regulation. Boston: Kluwer Academic Publishers, 2004.

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J, Dun Nae, Machado Benedito Honório, and Pilowsky P. M, eds. Neural mechanisms of cardiovascular regulation. Boston: Kluwer Academic Publishers, 2004.

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Kunos, George, and John Ciriello, eds. Central Neural Mechanisms in Cardiovascular Regulation. Boston, MA: Birkhäuser Boston, 1991. http://dx.doi.org/10.1007/978-1-4615-9834-3.

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Kunos, George, and John Ciriello, eds. Central Neural Mechanisms in Cardiovascular Regulation. Boston, MA: Birkhäuser Boston, 1992. http://dx.doi.org/10.1007/978-1-4684-9184-5.

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N, Tobin Jack, and Florida. Legislature. House of Representatives. Committee on Business & Professional Regulation., eds. Sunrise review of cardiovascular technology regulation. [Florida]: The Committee, 1994.

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M, Magro Albert, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Central and peripheral mechanisms of cardiovascular regulation. New York: Plenum Press, 1986.

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Magro, A., W. Osswald, D. Reis, and P. Vanhoutte, eds. Central and Peripheral Mechanisms of Cardiovascular Regulation. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-9471-0.

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Endoh, Masao, Martin Morad, Hasso Scholz, and Toshihiko Iijima, eds. Molecular and Cellular Mechanisms of Cardiovascular Regulation. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-65952-5.

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Larry & Horti Fairberg Workshop on Control and Regulation of Transport Phenomena in Biological Systems with Special Emphasis on the Cardiac System (5th 2007 Antalya, Turkey). Control and regulation of transport phenomena in the cardiac system. Boston: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2008.

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Book chapters on the topic "Cardiovascular regulation"

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Mancia, Giuseppe, Thomas F. Lüscher, John T. Shepherd, George Noll, and Guido M. Grassi. "Cardiovascular Regulation: Basic Considerations." In Cardiovascular Medicine, 1525–39. London: Springer London, 2007. http://dx.doi.org/10.1007/978-1-84628-715-2_73.

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Cechetto, David F. "Neuropathology and Cardiovascular Regulation." In The Nervous System and the Heart, 159–79. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-713-0_4.

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Myllylä, Vilho V., Juha T. Korpelainen, Uolevi Tolonen, Hannele Havanka, and Anne Saari. "Neuropathology and Cardiovascular Regulation." In The Nervous System and the Heart, 181–237. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-713-0_5.

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Sartori, Claudio, Stefano F. Rimoldi, Emrush Rexhaj, Yves Allemann, and Urs Scherrer. "Epigenetics in Cardiovascular Regulation." In Advances in Experimental Medicine and Biology, 55–62. Boston, MA: Springer US, 2016. http://dx.doi.org/10.1007/978-1-4899-7678-9_4.

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Mahley, Robert W. "Receptor-Mediated Regulation of Cholesterol Metabolism." In Cardiovascular Disease, 79–85. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5296-9_9.

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Katz, Arnold M. "Regulation of Cardiac Contraction and Relaxation." In Cardiovascular Medicine, 1189–200. London: Springer London, 2007. http://dx.doi.org/10.1007/978-1-84628-715-2_55.

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Pagliaro, Pasquale, Claudia Penna, and Raffaella Rastaldo. "Regulation of Cardiac Contraction Force." In Basic Cardiovascular Physiology, 109–32. New York: River Publishers, 2022. http://dx.doi.org/10.1201/9781003337294-7.

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Morimoto, Taketoshi, Akira Takamata, and Hiroshi Nose. "Central Venous Pressure and Cardiovascular Responses to Hyperthermia." In Temperature Regulation, 279–83. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-8491-4_45.

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Nilsson, S. "Central Cardiovascular Dynamics in Reptiles." In Mechanisms of Systemic Regulation, 159–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79666-1_7.

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Lakatta, Edward G. "Regulation of cardiac relaxation." In Developments in Cardiovascular Medicine, 481–511. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-011-3990-8_42.

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Conference papers on the topic "Cardiovascular regulation"

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Codrean, Alexandru, and Toma-Leonida Dragomir. "Stability analysis of cardiovascular regulation." In 2015 23th Mediterranean Conference on Control and Automation (MED). IEEE, 2015. http://dx.doi.org/10.1109/med.2015.7158741.

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Wu, G. Q., J. B. Xin, L. S. Li, C. Li, Y. Fang, and C. S. Poon. "Nonlinear Interaction of Voluntary Breathing and Cardiovascular Regulation." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1616527.

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Reinhart-King, Cynthia A., Keigi Fujiwara, and Michael R. King. "The Cardiovascular Microenvironment." In ASME 2007 5th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2007. http://dx.doi.org/10.1115/icnmm2007-30167.

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Endothelial cell response to the complex hemodynamic environment of the circulatory system is critical to the pathophysiological regulation of the cardiovascular system; however the mechanism by which this mechanical signal is transduced remains poorly understood. Recent in vivo evidence suggests that cells are capable of responding locally to shear stress, on the length scale of a single cell. Because of the complexity of the in vivo environment, we have designed and characterized an in vitro microchannel chamber with well-defined rheological conditions. This system is being used to investigate endothelial cell signaling response to shear stress, thereby bridging the gap between in vivo and in vitro observations.
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Codrean, Alexandru, and Toma-Leonida Dragomir. "Delay effect on cardiovascular regulation - a systems analysis approach." In 2015 European Control Conference (ECC). IEEE, 2015. http://dx.doi.org/10.1109/ecc.2015.7330951.

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Остроухова, Оксана Николаевна, Марина Валерьевна Лущик, and Ксения Евгеньевна Рыбалова. "PATHOPHYSIOLOGICAL ADRENAL PATHOLOGY TRANSFORMATIONS IN CARDIOVASCULAR SYSTEM." In Фундаментальные и прикладные исследования. Актуальные проблемы и достижения: сборник избранных статей Всероссийской (национальной) научной конференции (Санкт-Петербург, Май 2022). Crossref, 2022. http://dx.doi.org/10.37539/fipi328.2022.31.33.003.

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Изменения в работе желёз внутренней секреции неизбежно сказывается на всех органах и системах, и особенно на органах кровообращения. Это проявляется нарушением сердечного ритма, регуляции артериального давления, липидного обмена и многим другим. Transformations in the endocrine glands work inevitably affect all organs and systems, especially the circulatory organs. This is manifested by violation of heart rhythm, blood pressure regulation, lipid metabolism and many others.
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Jalali, Ali, C. Nataraj, Margaret Butchy, and Ali Ghaffari. "Feature Extraction and Abnormality Detection in Autonomic Regulation of Cardiovascular System." In ASME 2011 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2011. http://dx.doi.org/10.1115/detc2011-48617.

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The objective of this study is to develop an efficient methodology for classifying patients suffering any type of blood pressure dysregulation from healthy subjects. Four features of malfunctions in blood pressure regulation are introduced, and a criterion is proposed for each feature to evaluate and distinguish patients from healthy subjects. The evaluated features are based on the analysis of difference between data related to healthy subjects and those collected from patients. The proposed criteria are implemented on a group of healthy and patient subjects by collecting their systolic blood pressure (SBP) and their heart rate (HR) time series. The proposed method is applied on three different groups of subjects each containing four healthy and eleven patients. It is shown that the algorithm properly detects the status of all fifteen subjects in one group and fourteen subjects in two groups. The results obtained indicate that the selected features have remarkable capability in detection of blood pressure dysregulation.
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Baselli, Giuseppe, Federico Aletti, and Manuela Ferrario. "Respiration in cardiovascular regulation models: Signal or confounding factor? A review." In 2014 8th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2014. http://dx.doi.org/10.1109/esgco.2014.6847606.

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Wang, Lang, Zhipei Huang, Jiankang Wu, Yu Meng, and Rongjing Ding. "A model-based method to evaluate autonomic regulation of cardiovascular system." In 2015 IEEE 12th International Conference on Wearable and Implantable Body Sensor Networks (BSN). IEEE, 2015. http://dx.doi.org/10.1109/bsn.2015.7299374.

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Gal-on, B., I. Brown, and A. Nunn. "Monitoring and Assessment of Cardiovascular Regulation in Spinal Cord Injured Patients." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1616081.

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Campesino, Laura Martinez, Jessica Johnston, Endre Kiss-Toth, and Heather Wilson. "114 TRIB3-mediated regulation of macrophage phenotype." In British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.113.

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Reports on the topic "Cardiovascular regulation"

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Yahav, Shlomo, John McMurtry, and Isaac Plavnik. Thermotolerance Acquisition in Broiler Chickens by Temperature Conditioning Early in Life. United States Department of Agriculture, 1998. http://dx.doi.org/10.32747/1998.7580676.bard.

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The research on thermotolerance acquisition in broiler chickens by temperature conditioning early in life was focused on the following objectives: a. To determine the optimal timing and temperature for inducing the thermotolerance, conditioning processes and to define its duration during the first week of life in the broiler chick. b. To investigate the response of skeletal muscle tissue and the gastrointestinal tract to thermal conditioning. This objective was added during the research, to understand the mechanisms related to compensatory growth. c. To evaluate the effect of early thermo conditioning on thermoregulation (heat production and heat dissipation) during 3 phases: (1) conditioning, (2) compensatory growth, (3) heat challenge. d. To investigate how induction of improved thermotolerance impacts on metabolic fuel and the hormones regulating growth and metabolism. Recent decades have seen significant development in the genetic selection of the meat-type fowl (i.e., broiler chickens); leading to rapid growth and increased feed efficiency, providing the poultry industry with heavy chickens in relatively short growth periods. Such development necessitates parallel increases in the size of visceral systems such as the cardiovascular and the respiratory ones. However, inferior development of such major systems has led to a relatively low capability to balance energy expenditure under extreme conditions. Thus, acute exposure of chickens to extreme conditions (i.e., heat spells) has resulted in major economic losses. Birds are homeotherms, and as such, they are able to maintain their body temperature within a narrow range. To sustain thermal tolerance and avoid the deleterious consequences of thermal stresses, a direct response is elicited: the rapid thermal shock response - thermal conditioning. This technique of temperature conditioning takes advantage of the immaturity of the temperature regulation mechanism in young chicks during their first week of life. Development of this mechanism involves sympathetic neural activity, integration of thermal infom1ation in the hypothalamus, and buildup of the body-to-brain temperature difference, so that the potential for thermotolerance can be incorporated into the developing thermoregulation mechanisms. Thermal conditioning is a unique management tool, which most likely involves hypothalamic them1oregulatory threshold changes that enable chickens, within certain limits, to cope with acute exposure to unexpected hot spells. Short-tem1 exposure to heat stress during the first week of life (37.5+1°C; 70-80% rh; for 24 h at 3 days of age) resulted in growth retardation followed immediately by compensatory growth" which resulted in complete compensation for the loss of weight gain, so that the conditioned chickens achieved higher body weight than that of the controls at 42 days of age. The compensatory growth was partially explained by its dramatic positive effect on the proliferation of muscle satellite cells which are necessary for further muscle hypertrophy. By its significant effect of the morphology and functioning of the gastrointestinal tract during and after using thermal conditioning. The significant effect of thermal conditioning on the chicken thermoregulation was found to be associated with a reduction in heat production and evaporative heat loss, and with an increase in sensible heat loss. It was further accompanied by changes in hormones regulating growth and metabolism These physiological responses may result from possible alterations in PO/AH gene expression patterns (14-3-3e), suggesting a more efficient mechanism to cope with heat stress. Understanding the physiological mechanisms behind thermal conditioning step us forward to elucidate the molecular mechanism behind the PO/AH response, and response of other major organs. The thermal conditioning technique is used now in many countries including Israel, South Korea, Australia, France" Ecuador, China and some places in the USA. The improvement in growth perfom1ance (50-190 g/chicken) and thermotolerance as a result of postnatal thermal conditioning, may initiate a dramatic improvement in the economy of broiler's production.
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