Abstract
Besides the fact that prolonged whole-body ischemia causes tissue and organ injury during cardiac arrest, additional damage occurs after the restoration of spontaneous circulation, during which the reperfusion activates a host of intracellular responses. These responses may lead to an increased threshold of oxidant-mediated injury and redox-mediated programed cell death in the stunned myocardium. The aim of this article is to summarize the major intracellular responses occurring from the onset of cardiac arrest until the post-resuscitation period that may lead to redox-mediated programed death of myocardial cells.
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