Mechanisms of Vascular Disease PDF Download
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Author: Robert Fitridge
Publisher: University of Adelaide Press
ISBN: 1922064009
Category : Medical
Languages : en
Pages : 589
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Book Description
New updated edition first published with Cambridge University Press. This new edition includes 29 chapters on topics as diverse as pathophysiology of atherosclerosis, vascular haemodynamics, haemostasis, thrombophilia and post-amputation pain syndromes.
Author: Robert Fitridge
Publisher: University of Adelaide Press
ISBN: 1922064009
Category : Medical
Languages : en
Pages : 589
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Book Description
New updated edition first published with Cambridge University Press. This new edition includes 29 chapters on topics as diverse as pathophysiology of atherosclerosis, vascular haemodynamics, haemostasis, thrombophilia and post-amputation pain syndromes.
Author: Michel Félétou
Publisher: Morgan & Claypool Publishers
ISBN: 1615041230
Category : Science
Languages : en
Pages : 309
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Book Description
The endothelium, a monolayer of endothelial cells, constitutes the inner cellular lining of the blood vessels (arteries, veins and capillaries) and the lymphatic system, and therefore is in direct contact with the blood/lymph and the circulating cells. The endothelium is a major player in the control of blood fluidity, platelet aggregation and vascular tone, a major actor in the regulation of immunology, inflammation and angiogenesis, and an important metabolizing and an endocrine organ. Endothelial cells controls vascular tone, and thereby blood flow, by synthesizing and releasing relaxing and contracting factors such as nitric oxide, metabolites of arachidonic acid via the cyclooxygenases, lipoxygenases and cytochrome P450 pathways, various peptides (endothelin, urotensin, CNP, adrenomedullin, etc.), adenosine, purines, reactive oxygen species and so on. Additionally, endothelial ectoenzymes are required steps in the generation of vasoactive hormones such as angiotensin II. An endothelial dysfunction linked to an imbalance in the synthesis and/or the release of these various endothelial factors may explain the initiation of cardiovascular pathologies (from hypertension to atherosclerosis) or their development and perpetuation. Table of Contents: Introduction / Multiple Functions of the Endothelial Cells / Calcium Signaling in Vascular Cells and Cell-to-Cell Communications / Endothelium-Dependent Regulation of Vascular Tone / Conclusion / References
Author: Raouf A. Khalil
Publisher: Biota Publishing
ISBN: 1615041818
Category : Medical
Languages : en
Pages : 78
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Book Description
Vascular smooth muscle (VSM) constitutes most of the tunica media in blood vessels and plays an important role in the control of vascular tone. Ca2+ is a major regulator of VSM contraction and is strictly regulated by an intricate system of Ca2+ mobilization and Ca2+ homeostatic mechanisms. The interaction of a physiological agonist with its plasma membrane receptor stimulates the hydrolysis of membrane phospholipids and increases the generation of inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 stimulates Ca2+ release from the intracellular stores in the sarcoplasmic reticulum. Agonists also stimulate Ca2+ influx from the extracellular space via voltage-gated, receptor-operated, and store-operated channels. Ca2+ homeostatic mechanisms tend to decrease the intracellular free Ca2+ concentration ([Ca2+]i) by activating Ca2+ extrusion via the plasmalemmal Ca2+ pump and the Na+/Ca2+ exchanger and the uptake of excess Ca2+ by the sarcoplasmic reticulum and possibly the mitochondria. A threshold increase in [Ca2+]i activates Ca2+-dependent myosin light chain (MLC) phosphorylation, stimulates actin–myosin interaction, and initiates VSM contraction. The agonist-induced maintained increase in DAG also activates specific protein kinase C (PKC) isoforms, which in turn cause phosphorylation of cytoplasmic substrates that increase the contractile myofilaments force sensitivity to Ca2+ and thereby enhance VSM contraction. Agonists could also activate Rho kinase (ROCK), leading to inhibition of MLC phosphatase and further enhancement of the myofilaments force sensitivity to Ca2+. The combined increases in [Ca2+]i, PKC and ROCK activity cause significant vasoconstriction and could also stimulate VSM hypertrophy and hyperplasia. The protracted and progressive activation of these processes could lead to pathological vascular remodeling and vascular disease.
Author: J. Gordon Betts
Publisher:
ISBN: 9781947172807
Category :
Languages : en
Pages : 0
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Book Description
Author: Ronald J. Korthuis
Publisher: Morgan & Claypool Publishers
ISBN: 1615041834
Category : Medical
Languages : en
Pages : 147
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Book Description
The aim of this treatise is to summarize the current understanding of the mechanisms for blood flow control to skeletal muscle under resting conditions, how perfusion is elevated (exercise hyperemia) to meet the increased demand for oxygen and other substrates during exercise, mechanisms underlying the beneficial effects of regular physical activity on cardiovascular health, the regulation of transcapillary fluid filtration and protein flux across the microvascular exchange vessels, and the role of changes in the skeletal muscle circulation in pathologic states. Skeletal muscle is unique among organs in that its blood flow can change over a remarkably large range. Compared to blood flow at rest, muscle blood flow can increase by more than 20-fold on average during intense exercise, while perfusion of certain individual white muscles or portions of those muscles can increase by as much as 80-fold. This is compared to maximal increases of 4- to 6-fold in the coronary circulation during exercise. These increases in muscle perfusion are required to meet the enormous demands for oxygen and nutrients by the active muscles. Because of its large mass and the fact that skeletal muscles receive 25% of the cardiac output at rest, sympathetically mediated vasoconstriction in vessels supplying this tissue allows central hemodynamic variables (e.g., blood pressure) to be spared during stresses such as hypovolemic shock. Sympathetic vasoconstriction in skeletal muscle in such pathologic conditions also effectively shunts blood flow away from muscles to tissues that are more sensitive to reductions in their blood supply that might otherwise occur. Again, because of its large mass and percentage of cardiac output directed to skeletal muscle, alterations in blood vessel structure and function with chronic disease (e.g., hypertension) contribute significantly to the pathology of such disorders. Alterations in skeletal muscle vascular resistance and/or in the exchange properties of this vascular bed also modify transcapillary fluid filtration and solute movement across the microvascular barrier to influence muscle function and contribute to disease pathology. Finally, it is clear that exercise training induces an adaptive transformation to a protected phenotype in the vasculature supplying skeletal muscle and other tissues to promote overall cardiovascular health. Table of Contents: Introduction / Anatomy of Skeletal Muscle and Its Vascular Supply / Regulation of Vascular Tone in Skeletal Muscle / Exercise Hyperemia and Regulation of Tissue Oxygenation During Muscular Activity / Microvascular Fluid and Solute Exchange in Skeletal Muscle / Skeletal Muscle Circulation in Aging and Disease States: Protective Effects of Exercise / References
Author: Marilyn J. Cipolla
Publisher: Biota Publishing
ISBN: 1615047239
Category : Medical
Languages : en
Pages : 82
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Book Description
This e-book will review special features of the cerebral circulation and how they contribute to the physiology of the brain. It describes structural and functional properties of the cerebral circulation that are unique to the brain, an organ with high metabolic demands and the need for tight water and ion homeostasis. Autoregulation is pronounced in the brain, with myogenic, metabolic and neurogenic mechanisms contributing to maintain relatively constant blood flow during both increases and decreases in pressure. In addition, unlike peripheral organs where the majority of vascular resistance resides in small arteries and arterioles, large extracranial and intracranial arteries contribute significantly to vascular resistance in the brain. The prominent role of large arteries in cerebrovascular resistance helps maintain blood flow and protect downstream vessels during changes in perfusion pressure. The cerebral endothelium is also unique in that its barrier properties are in some way more like epithelium than endothelium in the periphery. The cerebral endothelium, known as the blood-brain barrier, has specialized tight junctions that do not allow ions to pass freely and has very low hydraulic conductivity and transcellular transport. This special configuration modifies Starling's forces in the brain microcirculation such that ions retained in the vascular lumen oppose water movement due to hydrostatic pressure. Tight water regulation is necessary in the brain because it has limited capacity for expansion within the skull. Increased intracranial pressure due to vasogenic edema can cause severe neurologic complications and death.
Author: John A Bevan
Publisher: Springer
ISBN: 1461475279
Category : Science
Languages : en
Pages : 376
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Book Description
Exactly sixty years ago Schretzenmayer provided the first experimental proof that changes in blood ftow can affect the diameter oflarge arteries. Since then, support has been growing for the idea that intraluminal blood ftow plays an important role in regulating not only the tone of blood vessels, but also their caliber and structure. Investigations of the&e phenomena have been given a strong impetus by the discovery that the endothelium can modulate the tone of underlying vascular smooth muscle via the release of a number of vasoactive substances. Investigators often diverge in their opinions regarding the nature of the vascular wall response to blood ftow and the mechanisms involved. This book is the first summary of our state of knowledge and the nature of the research carried out on ftow-related changes. Early chapters review involvement of shear-stress-dependent events in the circulation as a whole. They cover the biophysical principles of ftuid transport, the cellular signal transduction path ways, and the molecular biology and biochemistry of ftow-induced changes in endothelial cells. Later chapters provide an in-depth summary of the regula tion of vascular muscle tone by ftow. They include historical perspectives, evi dence that ftow-induced vasodilation is primarily endothelium-dependent and that it can induce constriction, and details on ftow-dependent regulation in regional vascular beds. Several chapters emphasize the endothelial activation by shear stress and its importance in the control offtow in the microcirculation.
Author: Margarethe Geiger
Publisher: Springer
ISBN: 3030122700
Category : Medical
Languages : en
Pages : 392
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Book Description
This well-structured textbook offers essential knowledge on the vascular system. The reader will learn the properties, basic cellular mechanisms and development of the different parts of the vascular system (including the heart), gain knowledge on vascular and related diseases, and will be made familiar with common and most current methods and techniques applied to analyze the vascular system in patients, in animal models, and ex vivo. This book is based on a PhD Course for students from various bioscientific backgrounds given at the Medical University of Vienna, and it will be a valuable resource for Master ́s Students in vascular biology and biomedicine in general and a helpful tool for young researchers world-wide wishing to gain or refresh their knowledge in this field.
Author: Lindsay Biga
Publisher:
ISBN: 9781955101158
Category :
Languages : en
Pages :
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Book Description
A version of the OpenStax text
Author: Michael Barany
Publisher: Elsevier
ISBN: 0080527892
Category : Science
Languages : en
Pages : 455
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Book Description
This valuable resource provides a systematic account of the biochemistry of smooth muscle contraction. As a comprehensive guide to this rapidly growing area of research, it covers the structure and characteristic properties of contractile and regulatory proteins, with special emphasis on their predicted function in the live muscle. Also included in this book are intermediate filament proteins, and desmin and vimentin, whose function in smooth muscle is unknown; and several enzymes involved in the phosphorylation-dephosphorylation of contractile and other proteins.
