Chapter category: Heart
Apoptosis in Ischemia - Reperfusion Injury
Ischemia-Reperfusion Injury in Cardiac Surgery
Edited by: Friedhelm BeyersdorfISBN: 1-58706-002-7
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Chapter authors:
Harald Darius, Waltraud Ibe and Michael Buerke
Apoptosis or "programmed cell death" has recently been recognized to be involved in several cardiovascular diseases. There are some histologic criteria as well as histochemical, biochemical and gel electrophoretic methods developed for the detection of apoptosis in isolated cells, tissues or organs. In myocarditis and heart failure evidence is accumulating that apoptosis may play a role in their pathophysiology. In isolated cardiomyocytes hypoxia and reoxygenation cause apoptosis, cytokines at physiologic concentrations induce apoptosis and intracellular promotors and inhibitors of apoptosis have been identified. In animal models of myocardial ischemia and reperfusion apoptotic cells have been detected in the area at risk not undergoing necrosis. Reperfusion itself either seems to induce apoptosis or at least significantly augments this process, depending on the experimental conditions and animal species studied. In autopsy studies of human myocardial infarction, victims apoptotic cells were identified in the border zone between successfully reperfused myocardium and the core ischemic area undergoing necrosis. Intracellular regulatory proteins (e.g., Bcl-2, Bax, Fas, p53) were identified to be involved in apoptosis induction or reduced expression. The pathophysiologic role of apoptosis in human myocardial infarction and reperfusion as well as in surgical ischemia and reperfusion still has to be determined. If the reduction or induction of apoptosis may be an useful therapeutic goal in the future to aim at is still unresolved.
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