Reperfusion of ischemic organs can result in tissue injury that is man
ifested as microvascular and parenchymal cell dysfunction. Reactive ox
ygen metabolites and polymorphonuclear leukocytes (PMN) have been impl
icated in the pathobiology of reperfusion injury. Reactive oxygen meta
bolites mediate the lipid peroxidation detected in postischemic tissue
s and promote the formation of inflammatory agents that recruit and ac
tivate PMN. These PMN appear to inflict reperfusion-induced tissue inj
ury. Drugs that scavenge or inhibit the formation of reactive oxygen m
etabolites and/or prevent the recruitment of PMN may be useful in the
treatment of reperfusion injury.