The occurrence and mechanisms of myocardial reperfusion injury have been demonstrated under a diverse array of experimental conditions by many groups of investigators. Observations by Hearse and colleagues (1, 2) demonstrated that the reintroduction of molecular oxygen to the previously hypoxic myocardium results in a sudden increase in irreversible tissue injury, a phenomenon termed the" oxygen paradox." The findings of Jolly et al (3) that the combined administration of superoxide dis mutase and catalase results in myocardial tissue salvage implied that toxic oxygen metabolites contribute to in vivo tissue injury beyond that mediated by ischemia alone.