Nitric Oxide Attenuates Neutrophil-Mediated Myocardial Contractile Dysfunction After Ischemia and Reperfusion

With the knowledge of NO as an antiadhesion molecule, we performed studies to investigate the effects of NO on postischemic polymorphonuclear leukocyte (PMN)-mediated myocardial contractile dysfunction. Studies were performed with isolated perfused rat hearts subjected to 20 minutes of global ischem...

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Bibliographic Details
Published in:	Circulation research Vol. 78; no. 1; pp. 65 - 72
Main Authors:	Pabla, Ravinder, Buda, Andrew J, Flynn, David M, Blesse, Steven A, Shin, Alice M, Curtis, Michael J, Lefer, David J
Format:	Journal Article
Language:	English
Published:	Hagerstown, MD American Heart Association, Inc 01-01-1996 Lippincott Lippincott Williams & Wilkins Ovid Technologies
Subjects:	Animals Biological and medical sciences Cardiology. Vascular system Cell Adhesion - drug effects Coronary heart disease Endothelium, Vascular - pathology Heart In Vitro Techniques Male Medical sciences Myocardial Contraction - drug effects Myocardial Ischemia - pathology Myocardial Ischemia - physiopathology Myocardial Reperfusion Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - physiopathology Neutrophils - pathology Neutrophils - transplantation Nitric Oxide - physiology Rats Rats, Sprague-Dawley Sydnones - pharmacology Vasodilator Agents - pharmacology Ventricular Function, Left - drug effects Cardiac performance Rat Rodentia Contractility Cardiovascular disease Coronary heart disease Myocardial disease Vascular disease Vertebrata Mammalia Reperfusion Ischemia Animal Nitrogen monoxide Myocardium Neutrophil
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Summary:	With the knowledge of NO as an antiadhesion molecule, we performed studies to investigate the effects of NO on postischemic polymorphonuclear leukocyte (PMN)-mediated myocardial contractile dysfunction. Studies were performed with isolated perfused rat hearts subjected to 20 minutes of global ischemia and 45 minutes of reperfusion. Human PMNs (50 million) were infused over the first 5 minutes of reperfusion, and the recovery of left ventricular function was compared with baseline values. Infusion of PMNs alone (n equals 10) led to a 61% reduction in left ventricular developed pressure (LVDP) and a 57% reduction in the pressure-rate product (PRP) at 45 minutes of reperfusion. Infusion of an NO donor, CAS-754 (n equals 9), resulted in 80.2 plus minus 6.7% recovery of LVDP and 77.0 plus minus 8.6% recovery of PRP. Treatment with L-arginine (2.5 mmol/L, n equals 10) resulted in a similar improvement in the postischemic contractile state of the heart. In contrast, N-nitro-L-arginine methyl ester (L-NAME) treatment (250 mu mol/L, n equals 10) resulted in an exacerbation of contractile dysfunction, as evidenced by a 93% reduction in LVDP at 45 minutes of reperfusion and a 91% reduction in PRP. The deleterious effects of L-NAME were prevented by L-arginine coperfusion. We failed to observe any cardioprotective effects when NO or L-arginine was administered to hearts subjected to 25 minutes of ischemia and 45 minutes of reperfusion in the absence of PMNs. In conclusion, PMN-mediated myocardial contractile dysfunction is attenuated by NO and exacerbated by blockade of NO synthesis.(Circ Res. 1996;78:65-72.)
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0009-7330 1524-4571
DOI:	10.1161/01.res.78.1.65