Myocardial injury mediated by oxygen free radicals.

Increasing evidence suggests that oxygen free radicals play a major role in the pathogenesis of reperfusion injury. Initial indirect evidence was based on beneficial effects of free radical scavengers administered exogenously at the time of postischemic reperfusion. Recent electron paramagnetic resonance (EPR) spectroscopy studies show a burst of oxygen-centered free radical generation during the first 60 seconds of reflow and administration of either a free radical scavenger, such as superoxide dismutase (SOD), or an iron chelator, such as deferoxamine, prevents this burst. The in vitro data obtained in a perfused rabbit heart model and the impressive reduction in infarct size, shown in an intact canine model, suggest that well-designed, randomized, placebo-controlled clinical trials of free radical scavengers and/or antioxidants should be performed to determine if postischemic reperfusion injury can be shown and/or prevented in humans.