Although many books deal with isolated problems of calcium disturbance in relation to cardiac and cerebral function, this is the first to focus specifically on calcium metabolism and cerebral ischemia. Internationally acknowledged experts present recent data and new concepts in an interdisciplinary approach to the subject. They examine basic information on the pathophysiology of cellular events, the damage caused by excitotoxic substances, and the effects of calcium antagonistic drugs as measured in experimental animals. These contributions may help lead to possible therapeutic interference for the prevention of calcium imbalance.

The human brain represents about 2% of the body weight, yet it accounts for approximately 20% of aerobic metabolism. This high dependency on energy-consuming processes is mainly caused by the active transport of ions, which is necessary to compensate for the transmembrane ion currents that are part ofthe complex signaling processes in the brain. Ninety-five percent ofthe brain's ATP is derived from mitochondrial oxidative phosphorylation. Since that organ' s storage capacity for oxygen is minimal, any interruption of oxygen delivery to brain cells willlead to changes in membrane excitability and, there fore, to disruption of neuronal signaling within seconds. It seems that mamma lian brain is especially vulnerable to such an interruption, since oxygen deprivation leads to activation of ion channel mechanisms in neurons that impair their communications. Thus, the function of the brain as a coordinator of vital homeostatic reflexes, and complex body reactions to external challenges, depends critically on the rate of oxygen delivery and oxygen consumption. Oxygen delivery depends on two variables described in the Fick relation ship: volume flow rate ofblood and the arterial oxygen content. A reduction in either of these two variables will have serious effects on vital brain func tions. Reduction of arterial blood flow to the brain can be caused by cardiac arrest, shock, carotid occlusion, Of hypotension (global ischemia). Oxygen content is progressively decreased in asphyxia (including drowning).

In this timely volume, eminent researchers provide detailed coverage of the relevant function of neurochemical correlates to cerebral ischemia as well as their pathophysiological significance.

A distinguished international panel of authors define our current understanding of neuronal damage after ischemia and critically review the significant recent developments and progress in cerebrovascular accident (CVA) drug trials, both in animal models and in the clinical setting. These leading basic and fundamental authorities survey such important new drugs as calcium-influx inhibitors, free-radical scavenging drugs, glutamate and glycinergic antagonists, and immune suppressors. They also evaluate all the latest findings concerning calcium homeostasis, glutamate toxicity, gene activation, and the role of free radicals, glycine, and hormones. Chapters devoted to the neuroimaging of stroke, clinical trials, and the role of cerebral immune activation complete this informative collection of cutting-edge reviews.

Proceedings of the Second International Symposium on Nimodipine, Miami Beach, Florida, USA, April 25-28, 1990

In this volume, one of a series of monographs devoted to the problems of cerebral ischemia and related topics, we present the proceedings of an international conference on Cerebral Ischemia and Basic Mechanisms held in Bad Schachen/Lake Constance, Germany in June 1992. The enormous progress in research recently on the basic mechanisms associated with cerebral ischemia has provided greater insight into the pathophysiological mechanisms of reduced brain perfusion and decreased cerebral metabolism. The high technology instrumentation used to unravel the intricacies of cerebral blood flow and metabolism includes positron emission tomography and magnetic resonance imaging. A description of sophisticated neurophysiological techniques will give the reader insight into new models of reversible and irreversible tissue damage and changes at the molecular level have been described. The therapeutic approaches which have developed from this re search have been or will be used in clinical trials and will open new avenues in the treatment of stroke. The organizers of the meeting would like to thank the advisory board for its helpful suggestions and the Deutsche Forschungsgemeinschaft and other sponsors for their important support.

This fascinating monograph is filled with information formerly found only in periodicals and symposia proceedings. Chapters discuss the different models of cerebral ischemia in use today, including their advantages and disadvantages. This one-of-a-kind resource also contains essential chapters on cellular mechanisms of ion and acid-base homeostases, and energy metabolism of the ischemic brain. It reviews the possible role of lipids, free fatty acids, and free radicals. Four chapters are devoted to neurotransmitters and neuroregulators in cerebral ischemia. This extraordinary work also covers aspects of protection against and resuscitation from cerebral ischemia. An extremely informative volume, this book is an absolute must for every student in the field of cerebral ischemia, as well as the clinician or scientist who is already involved with this worldwide problem.