• S A Padosch, P Vogel, and B W Böttiger.
• Klinik für Anaesthesiologie, Universitätsklinikum Heidelberg, Im Neuenheimer Feld 110, 69120 Heidelberg. stephan_padosch@med.uni-heidelberg.de
• Anaesthesist. 2001 Dec 1; 50 (12): 905-20.

AbstractNeuronal injury following cardiac arrest (global cerebral ischaemia) and stroke (focal cerebral ischaemia) is one of the major causes of the high morbidity and mortality associated with these pathological events. One of the major characteristics of this kind of neuronal injury is delayed neuronal degeneration. An increasing body of evidence indicates that apoptosis (programmed cell death) is involved in this process after global and focal cerebral ischaemia. In contrast to necrosis, which is primarily characterised by cellular metabolism failure and loss of membrane integrity, apoptosis represents a pattern of cell death in which an active energy-dependent cell death programme is initiated without any concomitant inflammatory reaction. Based on the knowledge that apoptosis plays a major role in delayed neuronal death following cerebral ischaemia, a variety of new neuroprotective therapeutic strategies have emerged (e.g. caspase inhibitors, viral anti-apoptotic proteins, modulation of systemic anti- and pro-apoptotic protein expression and death receptor antagonists). Many of these are still being experimentally evaluated. Relevant anti-apoptotic and neuroprotective therapeutic strategies could be introduced into clinical practice in the near future. The field of anaesthesiology will benefit from these important developments. New therapeutic opportunities might also become available in emergency medicine and critical care medicine. This article reviews the molecular basis of apoptosis and its physiological and pathophysiological relevance. The mechanisms of delayed neuronal death following focal and global cerebral ischaemia are presented with particular emphasis on the role of apoptosis. Based on this, possible future therapeutic interventions are highlighted and discussed.

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