The oxygen free radical system: potential mediator of myocardial injury.

The sequential univalent reduction of oxygen gives rise to very reactive intermediate products including superoxide anion radical, hydrogen peroxide and free hydroxyl radicals. Normally, the tissue concentration of these intermediate products of oxygen is severely limited; however, if oxygen free radicals are produced in excess of the capacity of the tissues to eliminate them, they may cause serious damage. The biochemistry and possible sources of free radical generation in animal models of ischemic/reperfusion injury are reviewed. The ability of scavengers of oxygen free radicals to improve mechanical, mitochondrial and sarcoplasmic reticulum function in animal models of ischemic/reperfusion injury suggests that oxygen free radicals are partly responsible for myocardial injury in these models. Future research should be directed at establishing the relevance of oxygen radical-mediated myocardial injury in the experimental setting to analogous clinical situations.