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Hypoxic conditioning suppresses nitric oxide production upon myocardial reperfusion.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ryou, Myoung-Gwi Sun, Jie Oguayo, Kevin N. Manukhina, Eugenia B. Downey, H. Fred Mallet, Robert T.
Description	Country affiliation: United States Author Affiliation: Ryou MG ( Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107-2699, USA.)
Abstract	Physiologically modulated concentrations of nitric oxide (NO) are generally beneficial, but excessive NO can injure myocardium by producing cytotoxic peroxynitrite. Recently we reported that intermittent, normobaric hypoxia conditioning (IHC) produced robust cardioprotection against infarction and lethal arrhythmias in a canine model of coronary occlusion-reperfusion. This study tested the hypothesis that IHC suppresses myocardial nitric oxide synthase (NOS) activity and thereby dampens explosive, excessive NO formation upon reperfusion of occluded coronary arteries. Mongrel dogs were conditioned by a 20 d program of IHC (FIO(2) 9.5-10%; 5-10 min hypoxia/cycle, 5-8 cycles/d with intervening 4 min normoxia). One day later, ventricular myocardium was sampled for NOS activity assays, and immunoblot detection of the endothelial NOS isoform (eNOS). In separate experiments, myocardial nitrite (NO(2)(-)) release, an index of NO formation, was measured at baseline and during reperfusion following 1 h occlusion of the left anterior descending coronary artery (LAD). Values in IHC dogs were compared with respective values in non-conditioned, control dogs. IHC lowered left and right ventricular NOS activities by 60%, from 100-115 to 40-45 mU/g protein (P < 0.01), and decreased eNOS content by 30% (P < 0.05). IHC dampened cumulative NO(2)(-) release during the first 5 min reperfusion from 32 +/- 7 to 14 +/- 2 mumol/g (P < 0.05), but did not alter hyperemic LAD flow (15 +/- 2 vs. 13 +/- 2 ml/g). Thus, IHC suppressed myocardial NOS activity, eNOS content, and excessive NO formation upon reperfusion without compromising reactive hyperemia. Attenuation of the NOS/NO system may contribute to IHC-induced protection of myocardium from ischemia-reperfusion injury.
File Format	HTM / HTML
ISSN	15353702
e-ISSN	15353699
DOI	10.3181/0710-RM-282
Journal	Experimental Biology and Medicine
Issue Number	6
Volume Number	233
Language	English
Publisher	Sage Publication
Publisher Date	2008-06-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Medicine Discipline Biology Anoxia Myocardial Reperfusion Myocardium Pathology Nitric Oxide Synthase Metabolism Nitric Oxide Animals Hematocrit Hemoglobins Ischemia Myocardial Reperfusion Injury Chemistry Nitric Oxide Synthase Type Iii Phosphorylation Reperfusion Time Factors Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry, Genetics and Molecular Biology

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