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Development of the vascular system of the bovine embryo to 40 days gestationByrnes, Wayne J January 2010 (has links)
Digitized by Kansas Correctional Industries
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Impact of diet on vascular function in patients with type II diabetes mellitusWong, Ching-yuen. January 2009 (has links)
Thesis (M.Res.(Med.))--University of Hong Kong, 2009. / Includes bibliographical references (p. 73-99).
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Effects of exercise training on pulmonary vasomotor responses in the pigJohnson, Lynelle January 2000 (has links)
Thesis (Ph. D.)--University of Missouri--Columbia, 2000. / Typescript. Vita. Includes bibliographical references (leaves 132-143). Also available on the Internet.
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Oldtidens lacre om hjerte, kar og puls en medicinak-historia studie mit einer deutschen Zusammenfassung.Gotfredzen, Edvard, January 1900 (has links)
Thesis--Københavns universitet. / Includes bibliographical references.
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Adaptive clutter filter design for micro-ultrasound color flow imagingof small blood vesselsCheung, Ka-hei., 張嘉熹. January 2010 (has links)
published_or_final_version / Electrical and Electronic Engineering / Master / Master of Philosophy
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Acute and chronic impact of pressure on vascular responsivenessZhao, Yingzi, 趙瑩子 January 2014 (has links)
Hypertension leads to vascular complications including endothelial dysfunction, heart failure and stroke. The purpose of the present studies was to investigate the chronic and acute impact of high pressure on vascular responsiveness.
In Study I, isometric tension measurements demonstrated that contractions to phenylephrine, in the presence of indomethacin (inhibitor of cyclooxygenase), were smaller in aortae of spontaneously hypertensive rats (SHR) with, than in those without, endothelium, while they were comparable in such preparations of normotensive Wistar-Kyoto rat (WKY); the difference in SHR aortae was not affected by L-NAME [inhibitor of nitric oxide synthase (NOS)]. This endothelium-dependent, NOS-independent inhibition of phenylephrine-induced contraction was greater in older SHR (36 versus 18 weeks), and abolished by NO scavengers and ODQ (inhibitor of soluble guanylyl cyclase). It was observed not only in the presence of indomethacin but also apocynin (antioxidant), but inhibited by diphenyleneiodonium (inhibitor of cytochrome P450 reductase). These results suggest that the endothelium-dependent, eNOS-independent inhibition is caused by NO produced by cytochrome P450 reductase in the endothelium of the SHR aorta.
Study II investigated the mechanisms underlying the reduced contractions to prostaglandin E2 [agonist of prostaglandin E2 and thromboxane-prostanoid (TP) receptors] by a previous exposure to phenylephrine (agonist of α1-adrenoceptor) in the aortic smooth muscle of the SHR. This inhibition induced by the pre-activation of α1-adrenoceptor was augmented in aortae of older SHR (36 versus 18 weeks) and was not present in WKY preparations. Pre-exposure to the protein kinase C (PKC) activator, phorbol 12,13-dibutyrate, also inhibited subsequent contractions to prostaglandin E2 in SHR aortae. Inhibition of PKC by calphostin C abolished the effect of pre-exposure to phenylephrine. The mRNA expressions of PKC isoforms differed in WKY and SHR smooth muscle. These experiments suggest that in the SHR but not the WKY aorta, α1-adrenergic activation causes heterologous desensitization of TP receptor through activation of a specific PKC isoform(s).
In Study III, experiments were performed in a pressure myograph to determine whether or not acute elevation of transmural pressure in the isolated carotid artery of adult mouse (10-12 weeks) impairs endothelium-dependent dilatation by increasing angiotensin II expression or by directly activating AT1 receptors. Transient exposure of arteries to increased pressure (150 mmHg, three hours) inhibited endothelium-dependent, NO-mediated dilatations to acetylcholine, but did not affect responses to the NO donor DETA-NONOate. Inhibiting angiotensin II signaling or angiotensin converting enzyme prevented the impairment of endothelium-dependent dilatation by elevated pressure. Elevated pressure increased the expression of angiotensinogen [precursor of angiotensin II]. Thus, exposure of carotid arteries to elevated pressure leads to local release of angiotensin II, which activates AT1 receptors to cause endothelial dysfunction.
In summary, chronic increased pressure increased the endothelial NO release produced by cytochrome P450 reductase from nitrate and developed the heterologous desensitization of TP receptor caused by PKC in SHR aorta. Acute increased pressure impaired endothelium-dependent NO-mediated vasodilatation by activation of local angiotensin system in adult mouse carotid artery. These processes likely contribute to the pathogenesis of hypertension-induced vascular dysfunction and organ injury. / published_or_final_version / Pharmacology and Pharmacy / Doctoral / Doctor of Philosophy
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Mechanisms of acute actions of 17B-estradiol in the vascular systemKeung, Wen-yee, Wendy., 姜韻兒. January 2001 (has links)
published_or_final_version / abstract / toc / Pharmacology / Master / Master of Philosophy
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A MICROSCOPIC ANALYSIS OF VASCULOGENESIS AND SEQUENTIAL DEVELOPMENT OF EXTRACELLULAR MATRIX IN EARLY CHICK EXTRAEMBRYONIC BLOOD VESSELSMurphy, Mark Edwin, 1949- January 1976 (has links)
No description available.
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The rat aortic ring model of angiogenesis in vitro as an assay for angiogenic modulators, the role of the matrix metalloproteinases in vessel formationBurbridge, Michael Frank January 2000 (has links)
No description available.
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Wild blueberries affect endothelium-dependant vasodilation in Sprague-Dawley and spontaneously hypertensive rats /Clark, Kateryna, January 2007 (has links) (PDF)
Thesis (M.S.) in Food Science and Human Nutrition--University of Maine, 2007. / Includes vita. Includes bibliographical references (leaves 90-116).
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