Redox-mediated programed death of myocardial cells after cardiac arrest and cardiopulmonary resuscitation

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.

Figure 1.

Activation of programed cell-death pathways during the cardiac arrest interval.

Figure 2.

Activation of programed cell death during the post-resuscitation period. PMC, protein kinase C family.