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1
McMurdo, Lorraine. "Endothelin in cardiovascular physiology and pathophysiology". Thesis, Queen Mary, University of London, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321680.
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Spratt, James Christopher Samuel. "Endothelin : cardiovascular pharmacology, physiology & pathophysiology". Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/23202.
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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.
4
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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Nyarko-Adomfeh, Charles. "Cardiovascular function in normal man". Thesis, University of Nottingham, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317595.
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Webb, D. J. "The endothelin system in human cardiovascular physiology and pathophysiology". Thesis, University of Edinburgh, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.663587.
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Section 1 is concerned with exploring pharmacological responses to the ET family of peptides, the sarafotoxin analogue peptides, and ET antagonists, in human blood vessels in vivo. This was amongst the first work with ET-1 in humans, and certainly the first to use the sarafotoxins, ET receptor antagonists and ET converting enzyme (ECE) inhibitors. After characterisation of the pharmacological tools, it was possible to show clearly that endogenous ET-1 plays a physiological role in the control of peripheral resistance and blood pressure in healthy humans, suggesting important clinical applications for these agents. It was also shown that the ETA receptor is the major vasocontrictor receptor and that the major role in health of the ETB receptor is endothelium-dependent vasodilatation, enhancement of which may contribute to the beneficial clinical attributes of ETA receptor antagonism. In addition, local ET-1 infusion in the forearm circulation was shown to be a system whereby the clinical efficacy of systematically administered ET receptor antagonists could be modelled pharmacodynamically. Section 2-4 cover work confirming the substantial clinical utility of ET receptor antagonists and ECE inhibitors as vasodilators, particularly in essential hypertension, heart failure and renal failure. Other work, following congenital heart surgery, suggests that a cautious approach may be needed in some cases of pulmonary hypertension. Studies with neutral endopeptidase (NEP) inhibitors show unequivocally, but unexpectedly, that these agents are peripheral vasoconstrictors, and the evidence presented is consistent with this effect occurring because endogenously generated vascular ET-1 is an important substrate for NEP. Section 5 contains some miscellaneous but related studies, together with a series of review articles written from 1991-98 synthesising the literature at each stage and drawing conclusions about potential areas of major clinical interest in cardiovascular disease.
7
Muntean, Brian. "Roles of Primary Cilia in Cardiovascular and Renal Physiology". University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1396014586.
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McIntosh, Matthew. "Long-term cardiovascular adaptations to neonatal hypoxia". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110447.
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INTRODUCTION: Previous work from the Rohlicek laboratory has shown that neonatal hypoxia is associated with an increase in systolic blood pressure in two month old male rats. We have asked here whether this increase persists into later maturity, and if it is also present in females. We have further examined separately whether sex hormones or alterations in autonomic control are implicated in this increase. METHODS: Experiments were conducted on adult Sprague Dawley rats of both sexes. An experimental group was raised in hypoxia (FiO2 = 0.12) for the first ten days of life and subsequently raised in normoxia. A second group was reared entirely in normoxia. A subset of males and females were gonadectomized one month prior to recording. At two, three, and six months the rats were instrumented with an intravascular telemetric blood pressure transmitter monitoring abdominal aortic pressure. One week later arterial pressure was recorded for 24 hours in the ambulatory, unrestrained rats. RESULTS: Systolic pressure was significantly higher in neonatally hypoxic male rats at every age during their active (night-time) period and as well at 3 and 6 months during the resting (daytime) period compared to controls. The effect size of neonatal hypoxia increased with age, although this increase did not achieve significance. Neonatally hypoxic females did not show any differences in systemic pressure compared to controls. Castration did not prevent the development of elevated blood pressure in two month neonatally hypoxic males, nor did ovariectomy unveil any differences between neonatally hypoxic and control females at three months of age. In two month male rats hypoxic neonatally, baroreflex sensitivity was significantly decreased during their active (night-time) period. CONCLUSIONS: Our results indicate that the increase in blood pressure experienced by neonatally hypoxic adult male rats persists into later maturity. This effect appears to be sex specific to male animals. The finding of decreased baroreflex sensitivity following neonatal hypoxia at two months indicates that altered autonomic tone with a relative increase in sympathetic activity plays a role in the increase in arterial pressure.INTRODUCTION: Des travaux antérieurs entrepris au laboratoire Rohlicek ont montré que l'hypoxie néonatale est associée à une élévation de la pression artérielle systolique chez les rats mâles âgés de deux mois. Dans le cadre de la présente étude, on demande si cette élévation persiste plus tard dans la maturité et si elle est également présente chez les femelles. On essaye en outre de déterminer si les hormones sexuelles ou des altérations dans le contrôle autonome jouent un rôle dans cette élévation. MÉTHODE: Des études ont été menées sur des rats adultes Sprague-Dawley des deux sexes. Un groupe expérimental a été élevé en hypoxie (FiO2 = 0,12) durant les dix premiers jours de vie et subséquemment en normaxie. Un second groupe a été élevé entièrement en normaxie. Un sous-ensemble de mâles et de femelles ont été gonadectomisés un mois avant la prise de mesures. À deux, trois et six mois, des rats étaient branchés à un transducteur de pression artérielle intravasculaire avec télémétrie pour surveillance de la pression de l'aorte abdominale. Une semaine plus tard, la pression artérielle a été mesurée durant 24 heures chez des rats ambulatoires et non contenus. RÉSULTATS: La pression systolique a été considérablement plus élevée chez des rats mâles en hypoxie à tout âge durant leur période active (nocturne) et également à 3 et 6 mois durant la période de repos (diurne) par comparaison aux rats du groupe témoin. L'ampleur de l'effet de l'hypoxie néonatale s'est accrue avec l'âge, bien que cette augmentation n'ait pas été statistiquement significative. Les femelles en hypoxie néonatale n'ont montré aucune différence dans la pression artérielle générale par comparaison aux femelles du groupe témoin. Tout comme la castration n'a pu empêcher l'apparition d'une pression artérielle élevée chez les mâles en hypoxie néonatale âgés de deux mois, l'ovariectomie de même n'a pu montrer une quelconque différence entre les femelles en hypoxie néonatale par opposition aux femelles du groupe témoin à l'âge de trois mois. Chez les rats mâles âgés de deux mois en hypoxie néonatale, la sensibilité du baroréflexe a été considérablement atrophiée durant leur période active (nocturne). CONCLUSION: Nos résultats indiquent que l'élévation de la pression artérielle chez les rats mâles adultes en hypoxie néonatale persiste plus tard dans la maturité. Cet effet semble être spécifique selon le sexe chez les animaux mâles. La découverte de la sensibilité du baroréflexe atrophiée à la suite de l'hypoxie néonatale à deux mois indique que le tonus autonome altéré, conjugué à une augmentation relative de l'activité sympathique, jouent un rôle dans l'élévation de la pression artérielle.
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Bearham, D. A. "The cardiovascular consequences of burn injury". Thesis, University of Southampton, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374058.
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Sidery, Michael B. "The cardiovascular effects of food ingestion in man". Thesis, University of Nottingham, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335380.
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Green, Lucy Rebecca. "Mechanisms of fetal cardiovascular responses to acute hypoxia". Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338743.
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Brindle, Ryan C. "Peripheral physiological mechanisms of cardiovascular stress reactivity". Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6428/.
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This thesis aimed to increase understanding of the underlying physiological sources of the substantial inter-individual variability in heart rate (HR) and blood pressure (BP) reactions to acute psychological stress. This aim was achieved using a multi-method approach that included meta-analysis, laboratory studies, and prospective secondary analysis of epidemiological data. Chapter 2 implicated beta-adrenergic sympathetic activation and parasympathetic withdrawal in the cardiovascular stress response and showed that autonomic changes vary as a function of stress task, age, and sex. Chapter 3 demonstrated that individual differences in a unique HR complexity marker accounted for a significant amount of the observed variance in HR reactivity and that this effect was independent of task performance and changes in autonomic activity and respiration. Chapter 4 revealed that individual differences in resting physiological allostatic load related to HR reactivity such that higher allostatic load indicated lower reactivity. Finally, in Chapter 5, multivariate cluster analysis of HR, systolic and diastolic BP reactivity resolved a large sample into four homogenous clusters, each displaying significantly different reactivity patterns and risk of hypertension at 5-year follow-up. The research reported in this thesis confirms already suspected physiological sources of individual difference but also reveals novel sources that deserve further inquiry.
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White, Christopher Iain. "Cardiovascular 11β-HSD1 : its role in myocardial physiology and pathophysiology". Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/23391.
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Glucocorticoid production by the adrenal gland is regulated by hypothalamicpituitary- adrenal (HPA) axis activity. Within cells, glucocorticoid levels are modulated by 11β-hydroxysteroid dehydrogenase (11β-HSD), which interconverts active and intrinsically inert glucocorticoids. Glucocorticoids have widespread physiological effects and, in the cardiovascular system, they play a crucial role in heart development and maturation, blood pressure control, and myocardial calcium cycling. Mice which are unable to regenerate the physiological glucocorticoid, corticosterone, from 11-dehydrocorticosterone due to deletion of the type 1 11β-HSD isozyme (11β-HSD1) have previously been shown to have smaller, lighter hearts but unaltered systolic function. Moreover, a single nucleotide polymorphism (SNP) in the Hsd11b1 gene has been associated with reduced left ventricular mass in humans, suggesting a role for 11β-HSD1 in regulating cardiac size. After myocardial infarction (MI), 11β-HSD1 deficient mice have an augmented inflammatory response, increased numbers of pro-reparative alternatively-activated macrophages in the heart, enhanced peri-infarct angiogenesis and improved cardiac function compared to C57BL/6 controls. However, the role of ‘cardiovascular’ 11β-HSD1 in the development of these phenotypes, both basally and after MI, is unknown. It was hypothesised that ‘cardiovascular’ 11β-HSD1 deficiency would result in smaller hearts, and that this selective deletion would lead to altered calcium handling protein expression and diastolic abnormalities. Furthermore, it was hypothesised that ‘cardiovascular’ 11β-HSD1 deletion would reproduce the beneficial post-MI phenotype previously seen in global 11β-HSD1 deficient mice. The first aim was to characterise the cardiac phenotype of mice with global deletion of 11β-HSD1 (DelI mice), and mice in which deletion is restricted to cardiomyocytes and vascular smooth muscle cells (SMAC mice). SMAC mice have ‘floxed’ 11β- HSD1 alleles and a Cre recombinase transgene inserted into the Sm22α gene. Sm22α is expressed in vascular smooth muscle cells, and transiently in cardiomyocytes during development. Thus, Cre expression in these cells results in deletion of exon three of the Hsd11b1 gene and gives rise to a non-functional protein. Controls for DelI mice were C57BL/6 mice, and controls for SMAC mice were their Cre- littermates. DelI, but not SMAC, mice have smaller, lighter hearts, which may be explained by their shorter cardiomyocytes measured following isolation using a Langendorff preparation. Cardiomyocyte cross-sectional area is unchanged. In vivo measurement of cardiac function using ultrasound imaging showed systolic function is comparable between DelI mice and SMAC mice and their respective controls. However, there is mild diastolic dysfunction in both DelI and SMAC mice, characterised by reduced E wave deceleration and an increased mitral valve deceleration time. This phenotype occurred following pharmacological inhibition of 11β-HSD1, by administration of UE2316, a selective 11β-HSD1 inhibitor, to adult C57BL6/SJL mice. While ventricular collagen content is unaltered in DelI, SMAC and UE2316-treated mice compared to their respective controls, expression of sarcoplasmic reticulum Ca2+ ATPase (SERCA) is reduced, suggesting that altered calcium handling, rather than changes in stiffness, may underlie this phenotype. The second aim was to determine whether the beneficial acute outcomes seen previously in 11β-HSD1 deficient mice after MI could be reproduced by selective cardiovascular deletion of the enzyme. Seven days after MI, compared to Cre- littermate controls, SMAC mice have similar peri-infarct angiogenesis, total macrophage and alternatively-activated macrophage infiltration into the heart, infarct size, ventricular dilatation and systolic function. This suggests 11β-HSD1 deletion in another cell type, or types, is responsible for the phenotype seen in global 11β-HSD1 deficient mice. The final aim was to assess the impact of global 11β-HSD1 deficiency and ‘cardiovascular’ 11β-HSD1 deletion on the development of heart failure, using magnetic resonance imaging to determine structure and function. Eight weeks after MI, mice globally deficient in 11β-HSD1 have attenuated expression of ANP and β- MHC, RNA markers of heart failure, and show attenuated pulmonary oedema, reduced chamber dilatation, preserved systolic function and smaller infarcts compared to control. None of these parameters are altered in SMAC mice relative to control. In conclusion, the data presented in this thesis shows that cardiovascular 11β-HSD1 influences physiological cardiac function, potentially through regulation of calcium handling. 11β-HSD1 in other cells influences cardiomyocyte length, resulting in smaller hearts in its absence. Despite this, global 11β-HSD1 deficiency prevents heart failure development after MI, suggesting that pharmacological inhibition of 11β-HSD1 may be of benefit in treating this condition. Cardiovascular 11β-HSD1 does not, however, account for the changes in infarct healing or remodelling associated with this beneficial outcome, therefore these effects must be related to 11β-HSD1 deficiency elsewhere, such as fibroblasts or myeloid cells.
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McNulty, Clare. "Ageing, inflammation and cardiovascular function". Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6541/.
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Age is associated with the development of multi-system function loss including the musculoskeletal, immune and cardiovascular system, as well as body composition changes. These age-related alterations lead to frailty development and disease progression, reducing quality of life. A major lifestyle change occurring in later years is reduced physical activity levels. This thesis sought to examine the associations between physical activity and multi-system function loss in a cohort of elderly individuals, and to better understand the neural mechanisms underpinning the circulatory responses to exercise. It was observed that high daily physical activity levels attenuate some but not all of the age-related changes in elderly individuals. High physical activity was associated with superior physical functioning, lower total body fat and visceral adiposity, and plasma plasminogen activator inhibitor 1 (PAI-1) concentrations. Left ventricular (LV) diastolic function was negatively associated with mean arterial pressure (MAP) and visceral adiposity, suggesting that elderly individuals with higher MAP and visceral adiposity may have inferior LV diastolic function. In terms of neural mechanisms related to circulatory responses to exercise, in models of metaboreflex over-activity whereby BP is elevated as observed in heart failure patients, left atrial systolic function is enhanced in order to maintain end-diastolic volume and SV.
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Odblom, Maria Pernilla. "The innervation and physiology of the cardiac tissue in squid". Thesis, University of Plymouth, 1997. http://hdl.handle.net/10026.1/2545.
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Cephalopods have one of the most sophisticated cardiovascular systems among the invertebrates; they have an enclosed high pressure blood system, characterised by a double circulation, with one main systemic heart and two gill hearts. The cephalopod cardiac tissues are basically myogenic, but there is evidence for both nervous and hormonal regulation of most parts of the cardiovascular system, although the details of the control systems remain unknown. This study investigated the physiology and innervation of the cardiac tissues of the squid Alloteuthis subulata, Loligo forbesii and L vulgaris. Histological staining techniques established that the cardiac organs in squid are innervated from the palliovisceral lobe of the brain via the paired visceral nerves. The nerves to the ventricle, branch off from each of the visceral nerves, close to a commissure that connects the two visceral nerves. The auricles of the systemic heart are innervated from a cardiac ganglion, situated at the base of the gills. Other branches, also given off at this level, innervate the lateral vena cava, afferent and efferent branchial blood vessels, branchial hearts and the muscular valve region between the branchial heart and afferent branchial vessel. Electron microscopical studies have shown the structure and number of fibres in these nerves. Pharmacological studies of isolated and perfused squid branchial hearts showed that acetylcholine had an inhibitory effect on cardiac activity, acting on both nicotinic and muscarinic receptors. An aminergic receptor system may be present in squid branchial hearts, although the transmitter substance is still unknown. The catecholamines adrenaline and noradrenaline excite the heart, although in an inconsistent manner. Whole cell patch clamp studies revealed that individual squid heart cells operated, using a combination of at least six different ionic currents; three outward potassium currents (delayed rectifier, A-current, calcium-activated current) and three inward currents (sodium current, L- and T -type calcium currents). An understanding of the functions of the various currents was obtained by recording electrically stimulated and spontaneous action potentials, using conventional intracellular recording and stimulation techniques. The ionic currents were isolated by applying known channel antagonists, and each antagonist's effect on the action potential was studied.
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Hooper, Justin Shane. "Cardiovascular Effects Evoked by Airway Nociceptive Reflexes in Healthy and Cardiovascular Diseased Rats". Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6258.
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Acute inhalation of airborne pollutants alters cardiovascular function and has been shown to have its greatest affects on individuals with pre-existing cardiovascular disease. Evidence suggests that pollutant-induced activation of airway sensory nerves via the gating of ion channels is critical to these systemic responses. Here, we have investigated the cardiovascular responses evoked by inhalation of AITC (TRPA1 agonist) and capsaicin (TRPV1 agonist) in healthy Sprague Dawley (SD) and Wistar Kyoto (WKY) rats, and cardiovascular diseased Spontaneously Hypertensive (SH) rats. Inhalation of the agonists by healthy SD and WKY rats caused significant bradycardia, atrio-ventricular (AV) block and prolonged PR-Intervals. Inhalation of TRP agonists caused differential cardiovascular responses in the cardiovascular diseased SH rats, such that the TRP agonists evoked brady-tachy with AV block and premature ventricular contractions (PVCs). Bradycardic responses to AITC were inhibited by the TRP channel blocker ruthenium red and the muscarinic antagonist atropine, but atropine did not prevent the tachycardic responses seen in the SH rats. Adrenergic inhibition with atenolol prevented the tachycardic responses, but did not prevent the bradycardic responses evoked by AITC in the SH rats. In healthy rats, AITC inhalation also caused a biphasic blood pressure response: a brief hypertensive phase followed by a hypotensive phase, while evoking hypertension in the SH rats. Atropine accentuated the hypertensive phase in all animals, while preventing the hypotension in the healthy animals. In all animals, AITC-evoked heart rate responses were not abolished by terazosin, the [U+F061]1 adrenoceptor inhibitor, which prevented the hypertensive responses. Anesthetics had profound effects on AITC-evoked bradycardia and AV block, which was abolished by urethane, ketamine and isoflurane. Nevertheless, AITC inhalation caused bradycardia and AV block in paralyzed and ventilated rats following pre-collicular decerebration. In conclusion, we provide evidence that activation of TRP channels expressed on nociceptive airway sensory nerves causes significant cardiovascular effects in healthy rats via reflex modulation of the autonomic nervous system (ANS), and that these effects are exacerbated in cardiovascular diseased rats.
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Robertson-Gray, Olivia Jane. "Studies on the role of GPR55 in cardiovascular physiology and pathophysiology". Thesis, Robert Gordon University, 2017. http://hdl.handle.net/10059/3127.
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Atherosclerosis is a multifactorial, chronic inflammatory condition characterised by endothelial dysfunction, hyperlipidaemia and the accumulation of fatty deposits within the tunica intima of medium-to-large sized muscular arteries. This disease can prove fatal with patients suffering lethal myocardial infarction or stroke. Recently, two studies investigating the role of G-protein-coupled receptor 55 (GPR55) in atherosclerosis reported conflicting results; one reported a pro-atherogenic role for GPR55 and the other, an anti-atherogenic role for this receptor. Interestingly, another study demonstrated that the activation of GPR55 by lysophosphatidylinositol (LPI) in cultured rat neonatal ventricular cardiomyocytes provokes distinct cellular functions that are dependent on the location of GPR55, leading to suggestions that GPR55 may regulate cardiomyocyte function at two cellular sites and be a potential therapeutic target for cardiac disorders. While it has been demonstrated that GPR55 is important in the maintenance of cardiac function of healthy mice, what is currently unknown is if GPR55 has a role in the cardiovascular remodelling and cardiac function of atherosclerosis prone mice. To address this, the present studies were conducted to investigate 1) the role of GPR55 in atherogenesis, 2) if GPR55 has a role in the cardiac function of mice suffering from atherosclerosis, 3) the signalling pathway by which LPI activates cardiomyocytes, 4) the impact of GPR55 activation on the outcome of myocardial ischaemia/reperfusion (I/R) injury and, 5) the signalling mechanisms by which GPR55 elicits any observed effects on the myocardium in response to such injury. Using C57BL/6 (wildtype; WT), apolipoprotein E knockout (ApoE-/-; mouse model of atherosclerosis), GPR55 knockout (GPR55-/-) and novel ApoE-/-/GPR55-/- mice, this study has established that in the presence of high fat feeding (to accelerate atherosclerosis), GPR55 has a complex role whereby it both regulates risk factors associated with atherosclerosis (i.e. body weight and fat mass) yet promotes the development of fatty streaks within the vasculature, via a lipid independent mechanism. In terms of cardiac function, GPR55 exerted a protective role by maintaining the systolic function of high fat fed ApoE-/- mice, yet negatively affected the contractile reserve of these mice. With regard to infarct size, the present study established that LPI-induced activation of GPR55 (pre-global ischaemia) exacerbates myocardial tissue injury via a Rho-associated protein kinase (ROCK) dependent mechanism. Finally, this study established that LPI signals through the same signalling pathway as it did in the isolated heart, in both mouse and human-induced pluripotent stem cell-derived cardiomyocytes thus suggesting a translational role for GPR55 in the human heart. In conclusion, despite further research being required, the data presented within this thesis provides evidence that GPR55 may have the potential to be targeted for therapeutic gains in atherosclerosis and myocardial I/R injury.
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GUALA, ANDREA. "Mathematical modelling of cardiovascular fluid mechanics: physiology, pathology and clinical practice". Doctoral thesis, Politecnico di Torino, 2015. http://hdl.handle.net/11583/2615064.
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The cardiovascular apparatus is a complex dynamical system that
carries oxygen and nutrients to cells, removes carbon dioxide and
wastes and performs several other tasks essential for life. The
physically-based modelling of the cardiovascular system has a long
history, which begins with the simple lumped Windkessel model by
O. Frank in 1899. Since then, the development has been impressive
and a great variety of mathematical models have been proposed.
The purpose of this Thesis is to analyse and develop two different mathematical models of the cardiovascular system able to
(i) shed new light into cardiovascular ageing and atrial fibrillation
and to (ii) be used in clinical practice. To this aim, in-house codes
have been implemented to describe a lumped model of the complete
circulation and a multi-scale (1D/0D) model of the left ventricle
and the arterial system. We then validate each model. The former is validated against literature data, while the latter against
both literature data and numerous in-vivo non-invasive pressure
measurements on a population of six healthy young subjects.
Afterwards, the confirmed effectiveness of the models has been
exploited. The lumped model has been used to analyse the effect
of atrial fibrillation. The multi-scale one has been used to analyse the effect of ageing and to test the feasibility of clinical use
by means of central-pressure blind validation of a parameter setting unambiguously defined with only non-invasive measurements
on a population of 52 healthy young men. All the applications
have been successful, confirming the effectiveness of this approach.
Pathophysiology studies could include mathematical model in their
setting, and clinical use of multi-scale mathematical model is feasible.
19
Gallacher, David John. "The role of the posterior cerebellar vermis in cardiovascular control". Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309284.
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Fardipour, Parvin. "Computer modelling of the human cardiovascular system based on relational analysis". Thesis, City University London, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328932.
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Sundblad, Patrik. "Effects of physical activity and gravitational stress on cardiovascular control /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3791-5/.
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Hawkley, Louise C. "Loneliness, psychosocial states, behavior, and cardiovascular physiology : a 12-hour field study /". The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486399160107369.
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Bagatto, Brian. "The Developmental Physiology of the Zebrafish: Influence of Environment and Cardiovascular Attributes". Thesis, University of North Texas, 2001. https://digital.library.unt.edu/ark:/67531/metadc2854/.
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Temperature effects on the development of the zebrafish embryos and larvae and adults were examined. It was found that the earlier in development a temperature change was performed on an embryo, the more significant the change in survival and/or subsequent development. Thus, viable temperature ranges for zebrafish widened significantly as development proceeded. Adults reared and bred at 25oC produced embryos that were significantly more successful at the lower range of rearing temperatures compared to embryos produced from adults reared at 28oC. The majority of this study focused on the physiological effects of swim training during development in the zebrafish. The earlier in development the zebrafish larvae were trained, the greater the mortality. Trained free swimming larvae had a significantly higher routine oxygen consumption after 11 days of training, and a higher mass specific routine metabolic rate after 8 and 11 days of training. Trained free swimming larvae consumed significantly less oxygen during swimming and were more efficient at locomotion, compared to control larvae. Training enhanced survival during exposure to extreme hypoxia in all age groups. Performance aspects of training were investigated in attempt to quantify training effects and in most cases, trained fish performed significantly better than controls. As blood vessels formed during development, they decreased in cross sectional area from days two to six. It was also shown that the variability in visual stroke volume measurements could be reduced significantly by using a third dimension in the analysis with a more accurate volume equation. Finally, the ontogeny of cardiac control was evaluated. The adrenergic receptors were the first to respond to pharmacological stimulation but were closely followed by cholinergic pharmacological stimulation a few days later. There was a significant cholinergic tone present in day 15 zebrafish larvae which persisted. Although an adrenergic tone was not documented in this study, this does not prove its lack of existence.
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Tuttle, Hillary Ann. "Inflammation in diabetic women with cardiovascular disease". Diss., The University of Arizona, 2003. http://hdl.handle.net/10150/289992.
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Diabetics have a much greater morbidity and mortality due to coronary heart disease (CHD) than non-diabetics. Furthermore, diabetic women have a 3.8 fold greater risk for CHD compared to diabetic men. Inflammation is now considered a risk factor for cardiovascular disease and also plays a role in diabetes. It is possible that diabetic women with cardiovascular disease (CVD) have a greater inflammatory response and increased interaction between white cells and platelets than diabetic men with CVD or non-diabetic women with CVD. This study tested the hypothesis that platelet-neutrophil conjugates, platelet activation, neutrophil activation, and cytokine production (interleukin-6 (IL-6), tumor necrosis factor (TNF-α), and interleukin-1 (IL-1β) are increased in diabetic women with CVD compared to diabetic men with CVD and non-diabetic women with CVD. Neutrophil activation was assessed by measuring the expression of neutrophil CD11b and the production of Reactive Oxygen Species (ROS). We found that the baseline expression of CD11b and ROS was not statistically different among any of the groups. Platelet activation was quantified by the expression of GPIIb/IIIa and P-selectin. We found that the baseline expression of GPIIb/IIIa was not significantly different among any of the groups. Diabetic women with CVD had a 2 fold greater expression of platelet P-selectin compared to diabetic women without CVD. We also found the platelet-neutrophil conjugate reactivity to platelet activating factor (PAF) was significantly increased by 60% in diabetic and non-diabetic women with CVD in comparison to diabetic men with CVD. Finally, we found that IL-6 was increased over fourfold in diabetic women with CVD compared to non-diabetic women. These results indicate that platelets are chronically activated and IL-6 is chronically elevated in diabetic women with CVD compared to diabetic women without CVD and may contribute to thrombosis and the greater severity of coronary heart disease observed in diabetic women. The platelet-neutrophil conjugates may contribute to thrombosis/inflammation and the greater severity of coronary heart disease observed in diabetic women as compared to diabetic men. These aspects of inflammation may indicate one of the processes that exacerbate cardiovascular disease in diabetic women.
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Gorr, Matthew W. "Air Pollution and Cardiovascular Dysfunction". The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1428674045.
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Journeay, William Shane. "Thermoregulatory and nonthermoregulatory interaction in human cardiovascular control". Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/26496.
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Purpose. Study #1 examined the responses to facial immersion under states of altered cardiac filling. Study #2 sought to examine changes in postexercise hemodynamics and skin blood flow (SkBF) when lower blood pooling was manipulated using lower body pressure. Methods. Study #1---Six male subjects participated. They performed 30-s apneic facial immersions under: LBNP, LBPP, during post-exercise hypotension (PEH); & Control. MAP, HR, and SkBF were measured. Study #2---Subjects were exposed to LBNP, LBPP; or no pressure after 15-mins of cycle exercise at 70% of VO2 peak. HR, CO, SV, MAP, TPR, & SkBF, skin and esophageal temperature were recorded. Conclusions. Study #1---Cardiac parasympathetic response during facial immersion can be attenuated when cardiac filling is compromised. Study #2---(1) LBPP accelerates recovery of baseline hemodynamics while LBNP exacerbates the postexercise hemodynamic state relative to control. (2) Altering postexercise hemodynamics via LBPP may affect thermal responses.
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Johnson, Darren A. "Cardiovascular responses to physical stressors in normotensive and exercise hypertensive individuals". Thesis, University of Ottawa (Canada), 1995. http://hdl.handle.net/10393/10100.
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This study compared the cardiovascular responses to the PWC 140, cold pressor test (CPT), and isometric hand grip (IHG), to evaluate the consistency in the blood pressure response among these physical stressors. Eighteen resting normotensive males were classified as either normotensive at exercise or exercise hypertensive on the basis of their blood pressure response to the first stage of the Canadian Aerobic Fitness Test (CAFT) for their age group. Subjects were administered a 6-min PWC 140 bicycle ergometer test, a 120 sec CPT (forearm and hand immersion), and a 120 sec IHG at 30% MVC. Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), heart rate (HR), stroke volume (SV), cardiac output (CO), and ejection fraction (EF) were recorded every 5 seconds during a one min resting period, during exercise, and for 3 min post exercise using a Finapress 2000 BP monitor and BoMed bioimpedance cardiac monitor. The results of this study indicate that: (1) there were no significant differences between the two groups for the cardiovascular responses to the PWC 140, IHG, and CPT with the exception of a greater CO and SV in normotensives on the PWC 140, and a higher HR in exercise hypertensives on the CPT; (2) the exercise hypertensives had a greater rate of increase in SBP and DBP than the normotensives over the first 90 seconds of the CPT; (3) there was no consistent pattern in the individual responses to the CAFT, CPT, and IHG with respect to $\Delta$SBP. It was concluded that within the context of this study, the blood pressure responses to dynamic exercise, isometric exercise, and cold stress were not consistent among the subjects and tests.
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Hanna, Brian Dale. "Control of sympathetic neuron and cardiovascular effector activity by carbon dioxide". Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75884.
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The effect of CO$ sb2$ on sympathetic preganglionic neuron (SPN) activity and hindlimb neurogenic vascular resistance (HVR) was investigated in cats. Both variables increased as continuous functions of systemic arterial PCO$ sb2$, from hypocapnia to hypercapnia. Eucapnic PCO$ sb2$ was responsible for a significant component of SPN background activity and HVR. The carotid body chemoreceptors were shown to contribute to the CO$ sb2$ response of SPNs, since section of the carotid sinus nerves, after prior section of the aortic nerves, reduced the CO$ sb2$ response of SPNs. A significant ventral medullary contribution to this CO$ sb2$ relationship was demonstrated, since the CO$ sb2$ response persisted after peripheral chemodenervation, was lost after acute spinal transsection and was markedly attenuated by cold-block of either the entire exposed ventral surface of the medulla or the specific bilateral area "S". Superficial ventral medullary chemoreceptor involvement was confirmed, since changes in HVR, comparable to those caused by altering arterial PCO$ sb2$, occurred with changes in the (H$ sp+$) and PCO$ sb2$ in artificial CSF perfusing these structures.
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Sun, Bing, i 孫冰. "Vestibular influence on central cardiovascular regulation in the rat: functional and anatomical aspects". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31244774.
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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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Wang, Lu Electrical Engineering & Telecommunications Faculty of Engineering UNSW. "Experimental investigation and mathematical modelling of human cardiovascular system during exercise". Awarded by:University of New South Wales. Electrical Engineering & Telecommunications, 2007. http://handle.unsw.edu.au/1959.4/40598.
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The hypothesis in this dissertation is that the mathematical and physiological models can be developed to estimate cardiac output and metabolic demand of exercising individual from simple non-invasive physiological parameters such as heart rate, respiration, working rate and body movement (using multiple triaxial accelerometers). The models developed could be incorporated as part of a closed loop control system for cardiac pacemaker and/or heart assist devices. A reliable measurement system has been developed to measure cardiac output, heart rate, body movement and respiratory variables and to process and analyze the data coming from the measurements. Analyzing, designing and modelling of the measurement system have also been conducted. The foremost is to model the mixing chamber based gas measurement system and the other is to analyze and compensate the orientation error of triaxial accelerometers on the assessment of energy expenditure. Two mathematical models and one physiological model have been developed in the current research. The first mathematical model is to estimate steady state energy expenditure using a nonlinear regression method from the outputs of triaxial accelerometers. Results show that the proposed nonlinear model is better than both the traditional linear models and the earlier nonlinear models. The second mathematical model emphasizes on investigating the key central cardiovascular response to the steady state of incremental exercise. The modeling results show that all the studied cardiovascular parameters response to exercise nonlinearly except heart rate which responses to exercise linearly. Furthermore, based on a previous model developed in the Biomedical Systems Laboratories in UNSW and the reliable experimental data, a physiological model has been established to successfully estimate both the cardiac output and the metabolic demand with heart rate and workload as its input.
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Nunn, Nicolas. "The role of the signalling protein XLalphas in cardiovascular control in mice". Thesis, University of Liverpool, 2012. http://livrepository.liverpool.ac.uk/9893/.
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Loss of the signalling protein XLαs in mice leads to a lean phenotype characterised by increased energy expenditure due to elevated sympathetic nervous system (SNS) stimulation of brown adipose tissue. XLαs is the protein produced from the Gnasxl transcript of the imprinted Gnas locus, and has a restricted expression pattern that includes a number of brain regions essential for SNS control of both energy expenditure and the cardiovascular system. However, it is unknown to what degree XLαs influences overall sympathetic tone, or how XLαs signalling in the brain causes these phenotypic changes. Using arterial cannulation, anaesthetised Gnasxl knockout mice had elevated blood pressure, shown to be caused by increased SNS stimulation by a greater blood pressure response to the sympatholytic reserpine in knockouts. Using electrocardiogram (ECG) telemetry, conscious Gnasxl knockout mice had elevated heart rate at night, as well as a significant heart rate response to both reserpine and the parasympatholytic atropine. This supported the previous results showing elevated SNS stimulation of the cardiovascular system, but paradoxically also suggested elevated parasympathetic stimulation. Therefore, autonomic control of the cardiovascular system was investigated in further detail by analysing heart rate variability (HRV). A number of HRV analyses were experimentally validated in wildtype mice. The most reliable method was the fast Fourier transform (FFT); high frequency (HF) power was used as a measure of parasympathetic activity, and low frequency (LF)/HF ratio was used as a measure of sympathetic activity. Gnasxl knockouts had a greater LF/HF response to reserpine, but an equivalent HF response to atropine, suggesting the mice had elevated SNS activity only. Additionally, knockouts had elevated LF/HF ratio at night, suggesting consistently elevated SNS output. Neuronal signalling pathways that may be deregulated in Gnasxl knockouts were investigated by injection of MTII and Exendin-4, agonists to the melanocortin 3/4 and GLP-1 receptors, respectively. Gnasxl knockouts had a hypersensitive heart rate response both to centrally injected MTII in anaesthetised mice and peripherally injected Exendin-4 in conscious mice. The hypersensitivity to Exendin-4 was investigated further by HRV analysis, which showed that Exendin-4 had no effect on the SNS, but caused a potent reduction in parasympathetic activity in both wildtypes and knockouts. Neuronal signalling changes in response to Exendin-4 were investigated by antibody staining for the early response gene c-fos. No significant differences were seen in overall numbers of activated neurones between wildtypes and knockouts in a number of brain regions including the nucleus of the solitary tract (NTS). Interestingly, neurones expressing XLαs showed no c-fos response to Exendin-4, except in the area postrema. In summary, loss of XLαs in mice resulted in elevated SNS stimulation of the cardiovascular system, as well as hypersensitivity to Exendin-4 that was unlikely to be caused by increased activation of XLαs-deficient neurones.
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Dunworth, William P. Caron Kathleen M. "Genetic mouse models elucidate the roles of adrenomedullin in cardiovascular development and physiology". Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2009. http://dc.lib.unc.edu/u?/etd,2832.
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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2009.Title from electronic title page (viewed Jun. 4, 2010). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Curriculum in Genetics and Molecular Biology." Discipline: Genetics and Molecular Biology; Department/School: Medicine.
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Penny, Daniel James. "Changes in integrated cardiovascular physiology during inotropic stimulation in the early postnatal period". Monash University, Institute of Reproduction and Development, 2004. http://arrow.monash.edu.au/hdl/1959.1/9661.
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Coccarelli, Alberto. "Understanding aspects of cardiovascular physiology and disease via a multi-physics modelling methodology". Thesis, Cardiff University, 2018. http://orca.cf.ac.uk/111464/.
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The overall aim of this study is to develop and analyse the performance of a multiscale framework involving arterial wall dynamics and blood flow in realistic vascular architectures that can facilitate the understanding of the onset and progression of vascular disease. This comprehensive modelling framework will also allow the virtual testing and ultimately inform the design of novel pharmacological probes. To achieve this aim, we need to deliver an arterial model able to account for i) the wall contractility triggered by biochemical processes at the cellular level ii) the interaction between the flow and vessel deformation, and iii) the transport phenomena along the arterial systemic circulation. For each problem component, a solution procedure has been proposed and validated against benchmark theoretical results and experimental measurements. First we characterised the structural behaviour of the arterial media layer and its response to the active contractile activity modulated by the smooth muscle Ca2+ dynamics. In this study, we modelled the activation, modulation and inhibition of the smooth muscle contraction by pharmacological interventions. Subsequently we have focused on the fluid structure interaction between wall mechanics and hemodynamics. This work required coupling a traditional incompressible arterial fluid model to a solid boundary, which represents the elastic arterial wall. The methodology proposed has been validated against a set of classical benchmark cases and exhibits improved numerical efficiency and significant memory savings. The third component of the work focuses on modelling transport and diffusion phenomena along the arterial branching network and within surrounding tissues. For the purpose of this study, a network of vessels was embedded within a solid tissue model of the human body. This model was able to predict how a property (in this application energy,but equivalently drug concentrations) is transported and diffused from the blood vessels to the tissues.
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Hammer, Fabian. "Corticosteroid hormone action in the cardiovascular system". Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1436/.
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The cardiovascular system (CVS) has emerged as an important target of corticosteroid hormones. Mineralocorticoid receptor antagonists provide cardiovascular protection and are now routinely used in disorders such as primary hyperaldosteronism, resistant hypertension and congestive heart failure (CHF) but the underlying molecular mechanisms of corticosteroid hormone action remain unclear. We have characterised corticosteroid hormone action and metabolism by 11β- hydroxysteroid-dehydrogenases (11β-HSDs) in isolated adult rat cardiomyocytes (CM) and cardiac fibroblasts (cFb). We have detected 11β-HSD1 expression and activity in CM and cFb where it facilitates glucocorticoid hormone action, whereas 11β-HSD2 was absent. We have shown differential gene regulation by aldosterone (Aldo) and corticosterone in CM and identified novel Aldo target genes which may provide insights into the molecular mechanisms of Aldo action. We have also studied the role of corticosteroids in essential hypertension and the effect of spironolactone (Spiro) upon their secretion and metabolism in patients with chronic kidney disease. We have shown that mineralocorticoids but not glucocorticoids are involved in elevated blood pressure in essential hypertension and that Spiro treatment results in compensatory activation of the renin-angiotensinaldosterone system (RAAS), whereas glucocorticoid secretion and metabolism remain unchanged. In summary, these data provide novel molecular and clinical insights into corticosteroid hormone action in the CVS.
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Brooke-Wavell, Katherine S. F. "Human body composition : measurement and relationship with exercise, dietary intakes and cardiovascular risk factors". Thesis, Loughborough University, 1992. https://dspace.lboro.ac.uk/2134/17193.
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This thesis describes studies related to human body composition, concentrating upon methodology of measurement, and a study on the influence of brisk walking programme upon healthy, previously sedentary middle-aged men. In chapter I, the principles of the techniques used for measurement of body composition in this thesis are discussed. The limitations and potential sources of error associated with each are discussed. The response of body composition to exercise, and the relationship of this response to changes in cardiovascular risk factors are considered. General methods are described in chapter 2. Techniques suitable for measurement of body composition in "field" conditions are evaluated in chapters 3 and 4. Near infra-red interactance was found to under-estimate fatness, to an increasing extent with increasing fatness. Bio-electrical impedance estimates of body composition from different sets of prediction equations from the literature differed significantly. Most overestimated fatness, to an increasing extent with increasing fatness. In chapter 5 techniques for measurement of subcutaneous adipose tissue are evaluated by comparison with A-mode ultrasound. Skinfold thicknesses were better correlated with subcutaneous adipose tissue thickness than were interactance data. Chapters 6 and 7 describe a year-long study on the effects of a brisk walking programme on healthy, previously sedentary middle-aged men. Volunteers were randomly allocated to walking or control groups (n = 42 and 23 respectively). Brisk walking for on average 27 minutes per day was not found to influence body composition, although significant changes in lower limb skinfold thicknesses were observed. The relationship of changes in blood pressure and blood concentrations of total cholesterol, lipoprotein-cholesterol subfractions and triglycerides with changes in body composition and fat distribution is examined. Energy intake did not change during the study, despite the expected increase in energy expenditure, and lack of change in body composition. Changes in dietary cholesterol and fatty acid intakes during the year are described, and related to changes in cardiovascular risk factors. In conclusion, newer field techniques were not found to be a better predictor of body composition than skinfold thicknesses. Participation in the walking programme did not significantly influence body composition or energy intake.
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Stevens, Sarah CW. "Calcium and Cancer: Implications for Cardiovascular Function and Disease". The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1337211154.
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Ade, Carl Jacob. "Cardiorespiratory and vascular function during stress". Diss., Kansas State University, 2013. http://hdl.handle.net/2097/15976.
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Doctor of PhilosophyDepartment of Anatomy and Physiology
Thomas J. Barstow
The primary aim of this dissertation was to evaluate the factors that contribute to the cardiorespiratory and vascular responses following exercise conditioning and microgravity deconditioning. The first study of this dissertation (Chapter 2) revealed that exercise training in the head down tilt posture, which places increases central blood volume compared to upright, results in cardiorespiratory adaptations in both upright and head down tilt postures which are not completely expressed with exercise training in the upright posture. These findings suggest that augmentation of the ventricular volume load during exercise training may result in adaptations that transfer across multiple body positions. In the second and third studies measurements of blood velocity and flow were performed via Doppler ultrasound. In Chapter 3 we observed that in the brachial and femoral arteries blood moves with a slightly blunted parabolic velocity profile that is very stable across a range of mean arterial pressures and downstream limb resistances. We concluded that these findings support the current calculations of shear rate based on the assumptions of laminar flow. With these assumptions confirmed, the investigation in Chapter 4 could be performed. We observed that acute exposure to a sustained antegrade shear rate, via unilateral forearm heating, increased measurements of flow-mediated dilation and the overall rate of adjustment for forearm blood flow and vascular conductance during dynamic handgrip exercise. These findings suggest that one potential stimulus for improvements in vascular function and health following exercise conditioning may be exposure to elevations in antegrade shear. Lastly in Chapter 5 we changed focus to the cardiorespiratory deconditioning following long-duration microgravity exposure. We retrospectively reviewed and analyzed previous investigations of microgravity deconditioning and demonstrated that the decrease in maximal O2 consumption ( O2max) occurs as a function of duration of exposure and that both convective and diffusive O2 transport pathways substantially contribute to this decline. In addition we reviewed the current literature and highlighted potential mechanisms, across several organ systems, which may contribute to this decline in O2max. Collectively, these studies revealed the breath of plasticity for cardiorespiratory adaptations to a variety of stressors.
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Rook, William. "The effects of chronic hypoxia in utero on cardiovascular regulation in the offspring". Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/3040/.
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A common consequence of the complications of pregnancy, such as preeclampsia, is reduced supply of nutrients, including oxygen, to the developing fetus. The consequences for the offspring are wide ranging, but include increased risk of cardiovascular disease. However, the mechanisms by which this occurs are poorly understood. Using a rodent model, this study has examined the regulation of blood vessels, particularly those supplying skeletal muscle, by local, endothelially-derived factors, and by the sympathetic nervous system, in adult rat offspring following chronic hypoxia in utero. The key findings include evidence that there are chronically high levels of oxidative stress in the skeletal muscle vasculature of the offspring. Further, the density of, and the activity in the sympathetic neurones supplying skeletal muscle blood vessels is markedly increased following chronic hypoxia in utero, but the vascular sensitivity to stimulation of these neurones is reduced. Following chronic hypoxia in utero, as the rats approached middle age, they became hypertensive relative to normal rats. Thus, the present study has offered some mechanistic insight, which adds to a growing body of literature, and which may help to explain why babies born of sub-optimal pregnancies are at higher risk of developing cardiovascular disease later in life.
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Williams, Daniel Patrick. "Dehydroepiandrosterone sulfate, resistive exercise training and cardiovascular disease risk factors in premenopausal females". Diss., The University of Arizona, 1993. http://hdl.handle.net/10150/186281.
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The present study was designed to test the hypothesis that endogenous serum levels of dehydroepiandrosterone sulfate (DHEAS) would be inversely related to cardiovascular disease (CVD) risk factors and that circulating concentrations ofDHEAS would increase along with favorable alterations in CVD risk factors as a result of resistive exercise training. Serum concentrations ofDHEAS, lipids, lipoproteins, and fasting insulin were determined along with estimates of total and regional body composition from anthropometry and dual-energy x-ray absorptiometry (DEXA) in a crosssectional sample of premenopausal females aged 28-39 years (N=96) and in a 12 month longitudinal subsample randomly assigned to exercise (n=27) and control (n=27) groups. The date of subject entry into the intervention trial ranged from mid-autumn to late winter. The percentage of total fat located on the trunk from DEXA (r=0.32, P=0.002) was positively correlated with DHEAS, whereas the percentage of total fat located on the legs from DEXA (r=-0.25, P=0.015) was inversely correlated with DHEAS after adjusting for age, smoking and fasting status. Because obesity may be a prerequisite for the metabolic aberrations commonly associated with fat distribution, subjects were also classified by DEXA-determined %Fat (≥30 vs < 30) as obese or nonobese. In obese but not nonobese women, indexes of upper body and/or truncal fat distribution were positively correlated (r=0.31 to 0.51, P < 0.05) with fasting insulin, triglycerides, total and LDL cholesterol and negatively correlated (r=-0.45, P < 0.01) with HDL cholesterol. Correlations of similar magnitude yet opposite in direction were observed between indexes of lower body or leg fat distribution and metabolic CVD risk factors. DHEAS was inversely related to and accounted for 9.0% of the variation in LDL cholesterol after controlling for upper and lower body fat distribution and fasting insulin. DHEAS was also positively related to and accounted for 6.8% of the variation in HDL cholesterol after controlling for truncal fat percentage and distribution. Over the 12 month intervention, 42 subjects (18 controls and 24 exercisers) gained lean tissue mass (LTM) and 12 subjects (9 controls and 3 exercisers) lost LTM, whereas 26 subjects (15 controls and 11 exercisers) gained fat mass (FM) and 28 subjects (12 controls and 16 exercisers) lost FM. After adjusting for baseline HDL cholesterol, hematocrit change and subject study entry date, mean HDL cholesterol levels were significantly (P=0.026) maintained to a greater extent in LTM gainers (-1.3%) than in LTM losers (-15.0%). The HDL cholesterol-maintaining effect of gaining LTM was independent of control or exercise group status (P=0.042) and of the change in FM (P=0.015). The following was concluded from the study: 1.) increased amounts of total fat located on the trunk, and decreased amounts of total fat located on the legs, are associated with increased serum DHEAS concentrations in normally menstruating females; 2.) increased DHEAS levels are associated with decreased LDL and increased HDL cholesterol levels after controlling for the common associations of DHEAS and lipoproteins with fat distribution in obese premenopausal females; and 3.) the gain in soft tissue lean mass may prevent reductions in HDL cholesterol levels associated with lean tissue mass loss in healthy premenopausal females.
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Mersereau, Eric, Cody Boyle, Shelby Poitra, Ana Espinoza, Joclyn Seiler, Robert Longie, Lisa Delvo i in. "Longitudinal Effects of Embryonic Exposure to Cocaine on Morphology, Cardiovascular Physiology, and Behavior in Zebrafish". MDPI AG, 2016. http://hdl.handle.net/10150/618721.
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A sizeable portion of the societal drain from cocaine abuse results from the complications of in utero drug exposure. Because of challenges in using humans and mammalian model organisms as test subjects, much debate remains about the impact of in utero cocaine exposure. Zebrafish offer a number of advantages as a model in longitudinal toxicology studies and are quite sensitive physiologically and behaviorally to cocaine. In this study, we have used zebrafish to model the effects of embryonic pre-exposure to cocaine on development and on subsequent cardiovascular physiology and cocaine-induced conditioned place preference (CPP) in longitudinal adults. Larval fish showed a progressive decrease in telencephalic size with increased doses of cocaine. These treated larvae also showed a dose dependent response in heart rate that persisted 24 h after drug cessation. Embryonic cocaine exposure had little effect on overall health of longitudinal adults, but subtle changes in cardiovascular physiology were seen including decreased sensitivity to isoproterenol and increased sensitivity to cocaine. These longitudinal adult fish also showed an embryonic dose-dependent change in CPP behavior, suggesting an increased sensitivity. These studies clearly show that pre-exposure during embryonic development affects subsequent cocaine sensitivity in longitudinal adults.
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Wang, Tse-Yao. "Impacts of Moderate Cold Exposure on Energy Metabolism, Obesity, and Cardiovascular Function". The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1384449386.
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Lamensdorf, Angela Mona-Lisa. "Cardiovascular risk and autonomic changes during high and low affect provocations". Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28098.
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Does having a positive family history of essential hypertension predispose one to greater cardiovascular reactivity? Could reactivity be assessed with stress tasks that have greater external validity than traditional laboratory stressors? To answer these questions? 2b subjects with parental history of essential hypertension and 3b subjects without) were induced to converse with an experimenter on (a) a neutral topic (the weather)? and (b) an affective topic (a frustrating person or event). The topics were selected from a Iist of 2b because they had been rated by undergraduates as being the least and most arousing topics to talk about with a stranger in an experimental situation. The ratings yielded no interactions of sex of experimenter with sex of the subject. Subjects also performed a mental arithmetic task which is a standard laboratory stressor. The order of task presentation was randomly assigned within groups but matched across groups and sex to control sequence effects. For each subject? a 15-minute base I ine period was al lowed before each task. Readings of blood pressure? heart rate and rate of respiration were made at minute one? three? and five of each task phase. Each conversation task consisted of five minutes of talking followed by Iistening for five minutes to the experimenter. The tasks were separated by five-minute intervals to allow return to baseline levels. Results indicated that compared to individuals without parental history of hyper tension? individuals with parental history displayed higher levels of blood pressure (but not heart rate and rate of respiration) whether talking or listening. When peak values were considered; positive parental history subjects showed greater reactivity to the affective topic on diastolic blood pressure. The results also indicated that the three kinds of stressors yielded different levels of physiological responses with the math task and talk phase of the affect task yielding higher levels of blood pressure and heart rate than talk about the weather. The difference between the math and affective tasks was not significant on systolic blood pressure? but math yielded higher responses on heart rate and lower responses on diastolic blood pressure than talking about a frustrating event or person. These results suggest that a more generalizabIe stress stimulus such as an affect-laden conversation? can be reasonably standardized across subjects and elicits an aIpha-adrenergic vaso-constrictive response? a response more readily given by individuals with positive parental history than individuals without. The results also suggest that individuals with positive parental history of hypertension have higher blood pressure levels than individuals without. With respect to the similarity of the findings of this study? with those of other studies which have used older populations? it is proposed that these results are generalizable to older populations and provide evidence that a positive family history of essential hypertension may be considered a risk factor for later cardiovascular disease.Arts, Faculty of
Psychology, Department of
Graduate
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Hemesath, Susan M. "Effects of acute aerobic exercise on cardiovascular reactivity to stress in healthy, untrained males". Thesis, This resource online, 1990. http://scholar.lib.vt.edu/theses/available/etd-06102009-063023/.
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Ayers, Misty. "EFFECTS OF HYPOXIC REARING ENVIRONMENT ON THE DEVELOPMENT, PHYSIOLOGY, AND ECOLOGY OF ZEBRAFISH". University of Akron / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=akron1153495631.
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Koon, Hon-wai Michael, i 管漢偉. "Role of endothelin-1 and nitric oxide on the cardiovascular function". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31245444.
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Hartwich, Doreen. "Neural cardiovascular control during exercise : influence of sex and ovarian hormones". Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3218/.
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Cardiovascular control during exercise results from three main mechanisms, namely central command (descending neural input), skeletal muscle afferent feedback (metabo - and mechanoreflex) and the arterial baroreflex. The studies outlined in this thesis sought to examine the potential sex- and ovarian hormone influences in neural cardiovascular control during exercise. It was observed that the activation of metabolically sensitive skeletal muscle afferents (i.e. muscle metaboreflex) by partial restriction of blood flow to the exercising skeletal muscle contributes to the exercise tachycardia via a reduction in cardiac baroreflex sensitivity from rest during dynamic exercise. Importantly, the magnitude of this metaboreflex-mediated reduction in cardiac baroreflex responsiveness was not different between men and women during the early and late follicular phases of the ovarian cycle. Baroreflex perturbation during dynamic exercise, by means of hypotensive and hypertensive stimuli to the carotid baroreceptors, revealed that baroreflex control of blood pressure was similarly maintained during exercise in men and women. Finally it was demonstrated that the sympathetic vasoconstriction in the exercising limb is similarly blunted in men and women. Overall, the results of this thesis suggest that there are no differences between men and women in baroreflex function and sympathetic vascular responsiveness during dynamic exercise.
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Nephew, Benjamin Charles. "Simultaneous modulation of behavioral, cardiovascular, and corticosterone responses to acute stress, with an emphasis on arginine vasotocin /". Thesis, Connect to Dissertations & Theses @ Tufts University, 2003.
Znajdź pełny tekst źródłaStreszczenie:
Thesis (Ph.D.)--Tufts University, 2003.Adviser: L. Michael Romero. Submitted to the Dept. of Biology. Includes bibliographical references (leaves 158-180). Access restricted to members of the Tufts University community. Also available via the World Wide Web;
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Barrett-O'Keefe, Zachary. "Cardiovascular control during exercise and the role of the sympathetic nervous system in heart failure with reduced ejection fraction". Thesis, The University of Utah, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10001028.
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The objective of this dissertation was to systematically investigate the hemodynamic response to exercise in heart failure with reduced ejection fraction (HFrEF) and healthy individuals of a similar age, with an emphasis on how the sympathetic nervous system (SNS) may contribute to the dysregulation of the cardiovascular system in this cohort. The first study aimed to determine how varying levels of metaboreceptor activation alters the mean arterial pressure (MAP) response as well as the degree in which cardiac output (CO) and systemic vascular conductance (SVC) contribute to the metaboreflex-induced increase in MAP. We observed similar increases in MAP induced by metaboreceptor activation in both groups; however, this response was driven primarily by increases in CO in the control group and reductions in SVC in the HFrEF group. These data suggest a preserved role of the metaboreflex-induced increase in MAP in HFrEF, but suggest that this response is governed by the peripheral circulation in this cohort, a maladaptation that may exacerbate systolic dysfunction through an increase in afterload. The second study of this dissertation was focused on investigating the peripheral vasodilatory and hyperemic response to exercise in isolation of central hemodynamic limitations in both the upper and lower limbs. This study documented an impaired hyperemic response to both static-intermittent handgrip exercise as well as dynamic single-leg knee-extensor exercise in HFrEF patients - impairments primarily attributed to vasodilatory dysfunction, as the increase in MAP induced by these exercise modalities was preserved compared to healthy individuals. Together, these findings have identified a significant attenuation of the exercise-induced hyperemic response during both upper and lower limb exercise, implicating maladaptions in the peripheral hemodynamic response to exercise as a potential contributor limiting exercise capacity in this patient group. The third study sought to address the contribution of the alpha-adrenergic receptor pathway in the regulation of blood flow to exercising skeletal muscle in HFrEF patients. At rest, alpha-1-adrenergic receptor vasoconstriction induced by local intra-arterial infusion of phenylephrine (PE) was reduced in HFrEF compared to control subjects. During exercise, the vasoconstrictor responsiveness to PE was significantly attenuated in the control group and preserved in HFrEF patients compared to rest. Additionally, nonspecific alpha-adrenergic receptor antagonism induced by local intra-arterial infusion of phentolamine increased blood flow to a greater degree in HFrEF compared to the control subjects, both at rest and during exercise. Together, these findings demonstrate a marked contribution of alpha-adrenergic receptor restraint of leg blood flow in HFrEF patients during exercise. Collectively, these three studies have provided new insight into the role the SNS and peripheral hemodynamics play in the maladaptive cardiovascular response to exercise displayed in patients with HFrEF, further implicating the peripheral expression of SNS activity as a primary contributor to impaired exercise capacity in this patient group.