Living organisms exhibit specific responses when confronted with sudden changes in their environmental conditions. The ability of the cells to acclimate to their new environment is the integral driving force for adaptive modification of the cells. Such adaptation involves a number of cellular and biochemical alteration including metabolic homeostasis and reprogramming of gene expression. Changes in metabolic pathways are generally short-lived and reversible, while the consequences of gene expression are a long-term process and may lead to permanent alternation in the pattern of adaptive responses. The heart possesses remarkable ability to adapt itself against any stressful situation by increasing resistance to the adverse consequences. Stress composes the foundation of many degenerative heart diseases including atherosclerosis, spasm, thrombosis, cardiomyopathy, and congestive heart failure. Based on the concept that excessive stress may play a crucial role in the pathogenesis of ischemic heart disease, attempts were made to design methods for preventing of myocardial injury. Creation of stress reactions by repeated ischemia and reperfusion or subjecting the hearts to heat or oxidative stress enables them to meet the future stress challenge. Repeated stress exposures adapt the heart to withstand more severe stress reactions probably by upregulating the cellular defense and direct accumulation of intracellular mediators, which presumably constitute the material basis of increased adaptation to stress. Thus, the powerful cardioprotective effect of adaptation is likely to originate at the cellular and molecular levels that compose fundamental processes in the prophylaxis of such diseases. Volume six of the Advances in Organ Biology series contains state-of-the-art reviews on myocardial preservation and cellular adaptation from the leading authorities in this subject.

Myocardial protection is regarded as one of the most important, yet also most controversial aspects of cardiac surgery. There has been considerable improvement in myocardial protection strategies over recent years, utilising a variety of new approaches to treat cardiac diseases, and this text is intended to embrace the state of the art in this field. The book summarises the state of knowledge on all aspects of myocardial protection, including the latest in the treatment of cardiac diseases, robotics, pediatric surgery and the treatment of cardiac failure. Robotic surgery, valvular surgery, pediatric surgery and coronary surgery are all covered by renowned experts, producing a comprehensive, forward-looking view of the field of myocardial protection. This book should function to update physicians and surgeons interested in the field of cardiac surgery on the current state of knowledge on myocardial protection.

In this volume, basic scientists, cardiologists and cardiac surgeons discuss all that is known about preconditioning/adaptation and how this state-of-the-art technique compares with conventional techniques of myocardial preservation, unveiling its mechanism of protection and potential clinical application.

During the past several years tremendous advancements have been made in the field of pharmacology and therapeutics. While new therapeutic strategies are coming up, old ones are being improved by modifications, or being replaced with newer ones. The major topics covered in this book include: endothelins, current topics in cardiovascular research, molecular pharmacology, recent developments in cancer research, antioxidants, oxidants and human disease, herbal drugs, developments in neuropharmacology, myelin biology and demyelinating disease, pharmacovigilance, role of cytokines in health and disease, ocular pharmacology, detoxification of xenobiotics-biotransformation and transport, and several other topics of current interest. The aim of this book is to fulfill the needs of the basic and clinical researchers as well as the students, particularly related to areas of current interest in pharmacology and therapeutics.

This book summarizes present knowledge of different mechanisms involved in the development of positive and negative consequences of cardiac adaptation. Particular attention is paid to the still underestimated adaptive cardiac responses during development, to adaptation to the frequently occurring pressure and volume overload as well as to cardiac changes, induced by enduring exercise and chronic hypoxia. Cardiac Adaptations will be of great value to cardiovascular investigators, who will find this book highly useful in their cardiovascular studies for finding solutions in diverse pathological conditions; it will also appeal to students, fellows, scientists, and clinicians interested in cardiovascular abnormalities.

Whenever the heart is challenged with an increased work load for a prolonged period, it responds by increasing its muscle mass--a phenomenon known as cardiac hypertrophy. Although cardiac hypertrophy is commonly seen under physiological conditions such as development and exercise, a wide variety of pathological situa tions such as hypertension (pressure overload), valvular defects (volume overload), myocardial infarction (muscle loss), and cardiomyopathy (muscle disease) are also known to result in cardiac hypertrophy. Various hormones such as catecholamines, thyroid hormones, angiotensin II, endothelin, and growth factors have also been shown to induce cardiac hypertrophy. Although the exact mechanisms underlying or pathological forrns of cardiac hypertrophy are poorly under the physiological stood, an increase in the intraventricular pressure is believed to represent the major stimulus for the development of cardiac hypertrophy. In this regard, stretching of the cardiac muscle has been shown to induce the hypertrophic response, but the role of metabolic influences in this process cannot be ruled out. Furthermore, different hormones and other interventions in the absence of stretch have been observed to stimulate protein synthesis in both isolated cardiomyocyte and vascular myocyte preparations. Nonetheless, it is becoming dear that receptor as well as phospholipid linked signal transduction pathways are activated in some specific manner depend ing upon the initial hypertrophic stimulus, and these then result in an increase in the size and mass of cardiomyocytes.