title: Evaluation of free radical injury in myocardium.
abstract: Abundant evidence now is available that free radicals are produced in excess when myocardium is reperfused following an episode of ischemia and that free radicals can injure myocytes and endothelial cells. Free radicals may contribute to either reversible or irreversible manifestations of cell injury from ischemia and reperfusion. Several investigators have observed that post-ischemic contractile dysfunction (myocardial stunning) can be attenuated by a variety of anti-free radical therapies, and there seems to be general agreement that free radical injury contributes to stunning. Whether free radicals are an important cause of lethal myocyte injury ("lethal reperfusion injury") remains controversial. Using similar interventions and animal models, both positive and negative results have been reported from a growing number of studies done to test the effect of anti-free radical therapies on infarct size. Proposed explanations include differences in: 1) dose of drug and onset or duration of treatment, 2) duration of occlusion or reperfusion, 3) methods of measuring infarct size or area at risk, and 4) failure of some studies to control for baseline variation in the major determinants of infarct size, e.g., collateral blood flow. At present, none of these explanations seems sufficient to resolve the question.
authors.affiliation: Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710.
authors.forename: K A
authors.initials: KA
authors.lastname: Reimer
authors.forename: M
authors.initials: M
authors.lastname: Tanaka
authors.forename: C E
authors.initials: CE
authors.lastname: Murry
authors.forename: V J
authors.initials: VJ
authors.lastname: Richard
authors.forename: R B
authors.initials: RB
authors.lastname: Jennings
mesh_terms: D000818:Animals; D005609:Free Radicals; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism
chemical_list: D005609:Free Radicals