Reperfusion of ischemic organs can result in tissue injury that is manifested as microvascular and parenchymal cell dysfunction. Reactive oxygen metabolites and polymorphonuclear leukocytes (PMN) have been implicated in the pathobiology of reperfusion injury. Reactive oxygen metabolites mediate the lipid per-oxidation detected in postischemic tissues and promote the formation of inflammatory agents that recruit and activate PMN. These PMN appear to inflict reperfusion-induced tissue injury. Drugs that scavenge or inhibit the formation of reactive oxygen metabolites and/or prevent the recruitment of PMN may be useful in the treatment of reperfusion injury.