title: Reperfusion injury.
abstract: This article reviews the early and late morphologic changes associated with reperfusion of ischemic myocardium. If instituted within minutes of coronary artery occlusion, all reversibly injured myocardium is salvaged. Once some irreversibly injured myocardium is present, the usually bland region of coagulation necrosis is transformed into an edematous, hemorrhagic zone with "contraction-band" necrosis and vascular obstruction (no-reflow phenomenon). Whether or not these changes occur in otherwise salvageable myocardium is controversial. Data from studies with conflicting results are presented. Popular proposed mechanisms of reperfusion injury include the no-reflow phenomenon and free radical-mediated injury. No reflow has been related to direct vascular injury, compression of capillaries by edema fluid, and obstruction of vascular channels by leukocytes. Free radicals, which inactivate enzymes and destroy membranes, are primarily oxygen derived, and produced by neutrophils, endothelial cells, and myocardial cells. Whether or not reperfusion injury exists is still debated; if it does, the mechanism of injury remains to be proven. Ongoing research in this field will augment our knowledge of cell death and interventions to delay or prevent it.
authors.affiliation: Department of Pathology, Cedars-Sinai Medical Center, UCLA School of Medicine 90048.
authors.forename: M C
authors.initials: MC
authors.lastname: Fishbein
mesh_terms: D005609:Free Radicals; D006801:Humans; D015428:Myocardial Reperfusion Injury / Q000473:pathology* / Q000503:physiopathology
chemical_list: D005609:Free Radicals