Published in 1991: This book explores the possibilities of protecting the heart against stress and ischemia through adaptation to intermittent hypoxia or to mild, nondamaging stress exposure. These possibilities are based on studies that show an increase in the potency and efficiency of stress-limiting systems when subjected to repeated stress actions, adaptation to high altitude hypoxia, or adaptation to increased physical loads. Any stress reaction is coupled with an activation of central and local stress-limiting systems, such as GABA-ergic, opioidergic, and serotonergic systems in the brain, as well as antioxidants, prostaglandins, and adenosine in executory organs. The book also presents the use of metabolites of stress-limiting systems rather than adaptation as a means to prevent cardiac arrythmias. It also discusses genetically determined deficiencies of stress-limiting systems and their role in the etiology of stress-induced diseases. Cardiologists and researchers studying stress and its effect on cardiovascular systems will find this book extremely useful.

Despite the considerable success in treating diseases of the heart and blood vessels, they still remain the major cause of mortality throughout the world. One of the reasons underlying this problem is our lack of understanding of the molecular and cellular aspects of the processes involved. These problems are fully discussed in Cellular Interactions in Cardiac Pathophysiology, which draws together 25 contributions from leading investigators from all parts of the world. The contributions are grouped under three headings: Extracellular matrix and cardiocyte interaction; Myocytic adaptations and myocardial injury; and Signal transduction.

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.

Pathophysiology of Cardiovascular Disease has been divided into four sections that focus on heart dysfunction and its associated characteristics (hypertrophy, cardiomyopathy and failure); vascular dysfunction and disease; ischemic heart disease; and novel therapeutic interventions. This volume is a compendium of different approaches to understanding cardiovascular disease and identifying the proteins, pathways and processes that impact it.

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.

This unique book presents an approach to viewing trauma. It examines the cellular consequences of trauma at a molecular level and provides new insights into the treatment of traumatic injury, based on cellular responses. The current of trauma research is reviewed, previously unpublished information on the topic is presented, and research directions are included.