A large number of cardiovascular diseases are accompanied by inflammation. This volume on the molecular basis of microcirculatory disorders gives a comprehensive summary of key steps in the inflammatory cascade. Leading investigators present a state-of-the-art analysis of the molecular determinants of leukocyte-endothelial cell adhesion, mechanotransduction in endothelial and inflammatory cells, mechanisms of cell activation, microvascular apoptosis with applications to ischemia-reperfusion in the brain, the heart and in venous disease, diabetes and hypertension. The book provides the latest thinking in these important cardiovascular problems, with the most contemporary literature and a look at the increasingly complex events during inflammation. Molecular biology tools, microvascular and modern bioengineering analysis are seamlessly integrated into the analysis of clinical problems. The book helps not only newcomers to gain entry into the interesting problems associated with microvascular disorders, but lays the foundation for the design of new therapeutic interventions.

In the past two decades a number of studies have shown that abnormalities in the function and structure of coronary microcirculation can be detected in several cardiovascular diseases. On the basis of the clinical setting in which it occurs, coronary microvascular dysfunction (CMD) can be classified into four types: CMD in the absence of any other cardiac disease; CMD in myocardial diseases; CMD in obstructive epicardial coronary artery disease; and iatrogenic CMD. In some instances CMD represents an epiphenomenon, whereas in others it represents an important marker of risk or may contribute to the pathogenesis of myocardial ischemia, thus becoming a possible therapeutic target. This book provides an update on coronary physiology and a systematic assessment of microvascular abnormalities in cardiovascular diseases, in the hope that it will assist clinicians in prevention, detection and management of CMD in their everyday activity.

The microcirculation is highly responsive to, and a vital participant in, the inflammatory response. All segments of the microvasculature (arterioles, capillaries, and venules) exhibit characteristic phenotypic changes during inflammation that appear to be directed toward enhancing the delivery of inflammatory cells to the injured/infected tissue, isolating the region from healthy tissue and the systemic circulation, and setting the stage for tissue repair and regeneration. The best characterized responses of the microcirculation to inflammation include impaired vasomotor function, reduced capillary perfusion, adhesion of leukocytes and platelets, activation of the coagulation cascade, and enhanced thrombosis, increased vascular permeability, and an increase in the rate of proliferation of blood and lymphatic vessels. A variety of cells that normally circulate in blood (leukocytes, platelets) or reside within the vessel wall (endothelial cells, pericytes) or in the perivascular space (mast cells, macrophages) are activated in response to inflammation. The activation products and chemical mediators released from these cells act through different well-characterized signaling pathways to induce the phenotypic changes in microvessel function that accompany inflammation. Drugs that target a specific microvascular response to inflammation, such as leukocyte-endothelial cell adhesion or angiogenesis, have shown promise in both the preclinical and clinical studies of inflammatory disease. Future research efforts in this area will likely identify new avenues for therapeutic intervention in inflammation. Table of Contents: Introduction / Historical Perspectives / Anatomical Considerations / Impaired Vasomotor Responses / Capillary Perfusion / Angiogenesis / Leukocyte-Endothelial Cell Adhesion / Platelet-Vessel Wall Interactions / Coagulation and Thrombosis / Endothelial Barrier Dysfunction / Epilogue / References

The microvasculature refers to the smallest blood vessels, arterial and venous, that nurture the tissues of each organ. Apart from transport, they also contribute to the systematic regulation of the body. In everyday terminology, the microcirculation is "where the action is." Microcirculation is directly involved in such disease states as Alzheimers, inflammation, tumor growth, diabetic retinopathy, and wound healing- plus cardiovascular fitness is directly related to the formation of new capillaries in large muscles. Microvascular Research is the first book devoted exclusively to this vital systemic component of the cardiovascular system and provides up to date mini-reviews of normal functions and clinical states. The contributing authors are senior scientists with international reputation in their given disciplines. This two-volume set is a broad, interdisciplinary work that encompasses basic research and clinical applications equally. * Broad coverage of both basic and clinical aspects of microvasculature research * Contains 167 chapters from over 300 international authors * Each chapter includes key figures and annotated references

This presentation describes various aspects of the regulation of tissue oxygenation, including the roles of the circulatory system, respiratory system, and blood, the carrier of oxygen within these components of the cardiorespiratory system. The respiratory system takes oxygen from the atmosphere and transports it by diffusion from the air in the alveoli to the blood flowing through the pulmonary capillaries. The cardiovascular system then moves the oxygenated blood from the heart to the microcirculation of the various organs by convection, where oxygen is released from hemoglobin in the red blood cells and moves to the parenchymal cells of each tissue by diffusion. Oxygen that has diffused into cells is then utilized in the mitochondria to produce adenosine triphosphate (ATP), the energy currency of all cells. The mitochondria are able to produce ATP until the oxygen tension or PO2 on the cell surface falls to a critical level of about 4–5 mm Hg. Thus, in order to meet the energetic needs of cells, it is important to maintain a continuous supply of oxygen to the mitochondria at or above the critical PO2 . In order to accomplish this desired outcome, the cardiorespiratory system, including the blood, must be capable of regulation to ensure survival of all tissues under a wide range of circumstances. The purpose of this presentation is to provide basic information about the operation and regulation of the cardiovascular and respiratory systems, as well as the properties of the blood and parenchymal cells, so that a fundamental understanding of the regulation of tissue oxygenation is achieved.

Ion Channels and Calcium Signaling in the Microcirculation, Volume 85, the latest release in the Current Topics in Membranes series, highlights the latest advances in the expression and function of ion channels and calcium signaling in vascular smooth muscle and endothelial cells in resistance arteries, arterioles and capillaries, critical components of microcirculation, the business end of the cardiovascular system. Leading experts have contributed chapters, including Smooth muscle ion channels and calcium signaling in the regulation of striated muscle arteriolar tone; Endothelial KIR channels as a key component of shear stress-induced mechanotransduction; Endothelial TRPV4 channels and vasodilator reactivity, and much more. Additional sections cover cerebral capillary endothelial TRPA channels and the regulation of blood flow; Endothelial mineralocorticoid receptors and the regulation of TRPV4 function in cerebral parenchymal arterioles in hypertension; Subcellular calcium signaling and myogenic tone development in the retinal microcirculation; Microvascular KIR channels: Basis, properties and regulation by lipid and hemodynamic forces, Ion channels and calcium signaling in capillary endothelial cells; Ion channels and calcium signaling in bladder arterioles and resistance arteries, and Myoendothelial feedback and endothelial IKCa and sKCa channels.

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.

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

Coronary Microvascular Obstruction in Acute Myocardial Infarction: From Mechanisms to Treatment provides a comprehensive understanding of the phenomenon of coronary microvascular obstruction (CMVO) that is the main limitation of reperfusion therapies in ST-elevation myocardial infarction. It provides in-depth coverage of the phenomenon of CMVO which heavily affects prognosis by increasing the risk of death and heart failure at follow-up. A first of its kind reference dedicated solely to this topic, it is appropriate for a wide audience, from researchers, to those who aid in the management, prevention and treatment of CMVO. - Provides in-depth coverage of coronary microvascular obstruction (CMVO), spanning research, management, prevention and treatment - Includes the most up-to-date information on CMVO as presented from top experts around the word - Provides access to a companion website with extra material, including tables, additional references and instructional videos - Gives extensive coverage on how to measure CMVO, including in-depth indexes that can be used to detect and quantify the phenomenon