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1 Internal Medicine, The Ohio State University, Columbus, Ohio, United States; Cardiology, Second Military Medical University, Shanghai, ShangHai, China
2 Internal Medicine, The Ohio State University, Columbus, Ohio, United States
3 the Davis Heart and Lung Research Institute and the Division of Cardiovascular Medicine, The Ohio State University College of Medicine, Columbus, Ohio, United States
* To whom correspondence should be addressed. E-mail: jay.zweier{at}osumc.edu.
While we have shown that endothelial nitric oxide synthase (eNOS)-derived NO down regulates mitochondrial oxygen consumption during early reperfusion, its effects on inducible NOS (iNOS) induction and myocardial injury during late reperfusion is unknown. Wild-type (WT) and eNOS -/- mice were subjected to 30 min of coronary ligation followed by reperfusion. Expression of iNOS mRNA and protein levels, and peroxynitrite production were lower in postischemic myocardium of eNOS-/- mice than that in WT mice 48 hrs post reperfusion. Significantly improved hemodynamics (+-dp/dt, LVSP, MAP), increased rate pressure product and reduced myocardial infarct size (18 +- 2.5% vs 31+-4.6%) were found 48 hrs after reperfusion in eNOS-/- mice compared to WT mice. Myocardial infarct size was also significantly decreased in WT mice treated with 1400W (20.5 +- 3.4%) compared to WT mice treated with PBS (33.9 +- 5.3%). A marked reperfusion-induced hyperoxygenation state was observed by electron paramagnetic resonance oximetry in postischemic myocardium, but PO2 values were significantly lower from 1 hr to 72 hrs in eNOS-/- than in WT mice. Cytochrome c oxidase activity and NADH-dehydrogenase (NADH-DH) activity were significantly decreased in postischemic myocardium in WT and eNOS-/- mice compared to baseline control respectively, and NADH-DH activity was significantly higher in eNOS-/- mice than in WT. Thus, deficiency of eNOS exerted a sustained beneficial effect on postischemic myocardium 48 hrs after reperfusion with preserved mitochondrial function, which appears to be due to decreased iNOS induction and decreased iNOS-derived peroxynitrite in postischemic myocadium.
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