Mechanisms of reperfusion injury.

Abstract	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 peroxidation 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.
Authors	B J Zimmerman, D N Granger
Journal	The American journal of the medical sciences (Am J Med Sci) Vol. 307 Issue 4 Pg. 284-92 (Apr 1994) ISSN: 0002-9629 [Print] United States
PMID	8160724 (Publication Type: Journal Article, Review)
Chemical References	Free Radical Scavengers Reactive Oxygen Species Xanthine Oxidase
Topics	Animals Cell Adhesion Free Radical Scavengers Humans Lipid Peroxidation Neutrophils (physiology) Reactive Oxygen Species (metabolism) Reperfusion Injury (drug therapy, physiopathology) Xanthine Oxidase (metabolism)

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