 | HEART IN STRESS
Copyright © 1999 by the New York Academy of Sciences
description
Annals of the New York Academy of Sciences 874:354-370 (1999)
© 1999 New York Academy of Sciences
Nitric Oxide and the Vascular Endothelium in Myocardial Ischemia-Reperfusion Injurya
JAKOB VINTEN-JOHANSENb,
ZHI-QING ZHAO,
MASANORI NAKAMURA,
JAMES E. JORDAN,
RUSSELL S. RONSON,
VINOD H. THOURANI AND
ROBERT A. GUYTON
Department of Surgery, Division of Cardiothoracic Surgery, The Cardiothoracic Research Laboratory, The Carlyle Fraser Heart Center, Crawford Long Hospital, Emory University School of Medicine, Atlanta, Georgia 30365, USA
aSupported in part by grant HL-46179 from the National Institutes of Health (National Heart, Lung, and Blood Institute), grant 97-30209N from the American Heart Association, by the Thoracic Surgery Foundation for Research and Education (V.H.T), and by the Carlyle Fraser Heart Center.
bAddress correspondence to: J. Vinten-Johansen, Ph.D., The Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center of Crawford Long Hospital, Emory University School of Medicine, 550 Peachtree Street N.E., Atlanta, Georgia 30365; Telephone: 404-686-2511; Fax: 404-686-4888; E-mail: jvinten{at}emory.edu
The normal coronary vascular endothelium (VE) tonically releases nitric oxide (NO) by converting L-arginine to citrulline by a constitutive NO synthase. Reperfusion after myocardial ischemia reduces basal and stimulated release of NO. This "vascular reperfusion injury" is mediated largely by neutrophils (PMN) through specific interactions between adhesion molecules on the endothelium and the PMN, an interaction that precedes myocyte injury. NO inhibits the PMN-mediated reperfusion injury by direct effects on both the PMN and the vascular endothelium. Cardioprotective strategies include augmentation of endogenous NO by the precursor L-arginine and the administration of exogenous NO donors at the time of perfusion, which (1) attenuates PMN adherence to the coronary artery and venous endothelium, (2) reduces PMN-mediated endothelial dysfunction, (3) reduces PMN accumulation in the area at risk, and (4) reduces infarct size. Hence, NO represents a powerful therapeutic tool with which to attenuate the consequences of ischemia-reperfusion injury on vascular injury and infarction.
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