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Role of endothelial dysfunction in the pathogenesis of reperfusion injury after myocardial ischemia
Author(s) -
Lefer Allan M.,
Tsao Philip S.,
Lefer David J.,
Ma XinLiang
Publication year - 1991
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.5.7.2010056
Subject(s) - pathogenesis , endothelial dysfunction , medicine , ischemia , cardiology , reperfusion injury , myocardial ischemia
Endothelial dysfunction occurs after myocardial ischemia and reperfusion characterized by a marked reduction in endothelium‐dependent relaxation (EDR) due to reduced release or action of endothelium‐derived relaxing factor (EDRF). This reduced EDR occurs in coronary rings isolated from cats 2.5 min after reperfusion and in isolated perfused cat hearts 2.5 min after reperfusion. No decrease in EDR occurs before reperfusion in either preparation, suggesting that this impairment in EDR occurs during reperfusion. The decrease in EDR occurs soon after the generation of superoxide radicals by the reperfused coronary endothelium. Accumulation of neutrophils and myocardial cell injury does not occur until 3–4.5 h after reperfusion. Thus, endothelial generation of superoxide radicals acts as a trigger mechanism for endothelial dysfunction which is then amplified by neutrophil adherence and diapedesis into the ischemic region enhancing post‐reperfusion ischemic injury. Agents that preserve endothelial function or inhibit neutrophil activation (e.g., superoxide dismutase, prostacyclin analogs, TGF‐ β , antibodies to adhesive proteins) can protect against endothelial dysfunction and myocardial injury, if administered before reperfusion.—Lefer, A. M.; Tsao, P. S.; Lefer, D. J.; Ma, X.‐1. Role of endothelial dysfunction in the pathogenesis of reperfusion injury after myocardial ischemia. FASEB J. 5: 2029–2034; 1991.