Endothelium-derived nitric oxide regulates postischemic myocardial oxygenation and oxygen consumption by modulation of mitochondrial electron transport

Nitric oxide (NO) production is increased in postischemic myocardium, and NO can control mitochondrial oxygen consumption in vitro. Therefore, we investigated the role of endothelial NO synthase (eNOS)-derived NO on in vivo regulation of oxygen consumption in the postischemic heart. Mice were subjec...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 2005-06, Vol.111 (22), p.2966-2972
Main Authors: XUE ZHAO, GUANGLONG HE, CHEN, Yeong-Renn, PANDIAN, Ramasamy P, KUPPUSAMY, Periannan, ZWEIER, Jay L
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Cell Respiration
Coronary heart disease
Disease Models, Animal
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
Electron Transport Complex IV - genetics
Heart
Male
Medical sciences
Mice
Mice, Knockout
Myocardial Ischemia - enzymology
Myocardial Ischemia - metabolism
Myocardial Ischemia - pathology
NADH Dehydrogenase - antagonists & inhibitors
Nitric Oxide - biosynthesis
Nitric Oxide - physiology
Nitric Oxide Synthase Type III - deficiency
Nitric Oxide Synthase Type III - metabolism
Oximetry
Oxygen - metabolism
Oxygen Consumption
Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis
Tyrosine - analogs & derivatives
Tyrosine - analysis
Up-Regulation
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Summary:Nitric oxide (NO) production is increased in postischemic myocardium, and NO can control mitochondrial oxygen consumption in vitro. Therefore, we investigated the role of endothelial NO synthase (eNOS)-derived NO on in vivo regulation of oxygen consumption in the postischemic heart. Mice were subjected to 30 minutes of coronary ligation followed by 60 minutes of reperfusion. Myocardial oxygen tension (Po2) was monitored by electron paramagnetic resonance oximetry. In wild-type, N-nitro-L-arginine methyl ester (L-NAME)-treated (with 1 mg/mL in drinking water), and eNOS knockout (eNOS-/-) mice, no difference was observed among baseline myocardial Po2 values (8.6+/-0.7, 10.0+/-1.2, and 10.1+/-1.2 mm Hg, respectively) or those measured at 30 minutes of ischemia (1.4+/-0.6, 2.3+/-0.9, and 3.1+/-1.4 mm Hg, respectively). After reperfusion, myocardial Po2 increased markedly (P
ISSN:0009-7322
1524-4539
DOI:10.1161/circulationaha.104.527226