Activation Metabolism And Perfusion Of The Heart

The basic mechanism underlying directional differences in excitability, con duction velocity, andsafetyfactor thatleadtocircusmovementreentry incardiac muscle is generally attributed to a spatial difference in the refractory period as originally described by Mines [1] or to a depressed segment as described by Schmitt and Erlanger [2]. A departure from this depolarization in cardiac muscle involve quantities, such as Vmax' that are not directly descriptive of the underlying mechanisms of propagation.

Assessment of cardiac energetics at the level of ATP-synthesis, chemomechanical energy transformation and whole organ dynamics as a function of haemodynamic load, ventricular configuration and oxygen- and substrates supply is basic to understanding cardiac function under physiological and pathophysiological (hypertrophy, hypoxia, ischaemia and heart failure) conditions. Moreover, cardiac energetics should be an important consideration in the choice and application of drugs especially in the case of vasodilators, inotropic agents and in cardioprotective measures. Only by considering energetics at the subcellular, cellular, and whole-heart level we can arrive at a better understanding of cardiac performance and ultimately better clinical judgement and drug therapy. Quantification of myocardial energetics will also help to determine the optimal time for surgical interventions such as valvular replacement or aneurysm resection. The present volume is the outcome of an international symposium on cardiac energetics held in Gargellen/Montafon (Austria), June 1986. The contributions will certainly help bridge the existing gap between basic research involving isolated structures and that involving the whole organ, on the one hand, and render the results derived from basic research applicable to clinical problems, on the other hand.

Research centering on blood flow in the heart continues to hold an important position, especially since a better understanding of the subject may help reduce the incidence of coronary arterial disease and heart attacks. This book summarizes recent advances in the field; it is the product of fruitful cooperation among international scientists who met in Japan in May, 1990 to discuss the regulation of coronary blood flow.

Taking the reader from an understanding of the basic mechanisms of heart failure through to an appreciation of the complexities of heart failure management and the remarkable improvements possible with good treatment, the Oxford Textbook of Heart Failure 2e covers all aspects necessary to manage a patient with heart failure. In full colour throughout, containing over 300 illustrations, and supported by detailed referencing from the huge evidence base that has developed over the last two decades, the textbook also includes extensive chapters on common co-morbidities. The new edition has been completely updated in line with new British and European Guidelines and contains new chapters on; Natriuretic Peptides and Novel Biomarkers in Heart Failure, The Future of Heart Failure, and Regenerative Therapies. Essential reading for consultant cardiologists and those in training, general physicians and those caring of the elderly, cardiothoracic surgeons, primary care doctors, pharmacists, and specialist nurses.

Pathophysiology of Heart Failure brings together leading basic scientists and clinicians, presenting new approaches to this complex problem, involving cardiomyopathic processes and ischemia perfusion injury. The result is a synthesis of state-of-the-art information on molecular biology, cellular physiology and structure-function relationships in the cardiovascular system. The role which excess intracellular calcium plays in the genesis of cardiac dysfunction is described as a fundamental mechanism underlying heart failure; one which may lead to improved prevention and treatment. Audience: Clinical and experimental cardiologists will find the book a helpful source of ideas and inspiration.

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

The study of cardiovascular function is vital to contemporary biomedical research. However, integration between cellular and subcellular research and organ-level studies is often lacking, as is integration of clinical and basic investigation. This book examines cardiovascular system function from the perspectives of assessment and analysis, with a focus on evaluating function at different anatomical levels using a combination of analytical, experimental, and clinical measurements.

Research at the molecular and the cellular level has greatly enhanced our understanding of the pathogenesis and management of heart disease. Valuable contributions, towards this end, have been made by scientists from different dis ciplines including biochemistry, physiology, pathology, molecular biology and biophysics. We felt that it would be of interest and value to bring together ex perts from diverse specialities to present their work and to discuss the common problems encountered in their endeavours. In accordance, a symposium was organised in February 1988 at the Postgraduate Institute of Medical Education & Research, Chandigarh. It was held during the annual meeting of the Indian section of the International Society for Heart Research. This book is a compila tion of some of the papers presented at the symposium. The symposium was sponsored by the Council on Cardiac Metabolism of the International Society and Federation of Cardiology. A number of Indian or ganisations gave generous financial help. These included the National Academy of Medical Sciences, Indian Council of Medical Research, Council of Scientific and Industrial Research and Department of Science and Technology. Desktop publishing was used to prepare this volume. In doing so we came to appreciate the remarkable qualities, skills and help rendered by Professor Dharam Vir. For typing the manuscripts and for other secretarial assistance we gratefully acknowledge the help of Ravinder and Sawtantar. PATHOPHYSIOLOGY AND PHARMACOLOGY OF HEART DISEASE 1 THE NEWBORN PIG HEART, A SUPERIOR ANIMAL MODEL OF CARDIAC HYPERTROPHY Howard E.