Protecting Mitochondrial Bioenergetic Function During Resuscitation from Cardiac Arrest

Successful resuscitation from cardiac arrest requires reestablishment of aerobic metabolism by reperfusion of tissues that have been deprived of oxygen for variable times. However, reperfusion concomitantly activates pathogenic mechanisms known as reperfusion injury. Mitochondria play a critical role as effectors and targets of such injury. Mitochondrial injury compromises oxidative phosphorylation and prompts release of cytochrome c to the cytosol and bloodstream, where it correlates with severity of injury. Novel and clinically relevant strategies to protect mitochondrial bioenergetic function are expected to attenuate injury at the time of reperfusion and enhance organ viability, ultimately improving resuscitation and survival from cardiac arrest.