Nitric oxide inhibition improved myocardial metabolism independent of tissue perfusion during ischemia but not during reperfusion

Nitric oxide (NO) is one of the important regulators of cardiac metabolism and function as well as of tissue perfusion. Myocardial NO formation is inc reased during ischemia and reperfusion. We investigated the roles of endoge nous NO in myocardial metabolism during ischemia and reperfusion independen t of tissue perfusion changes. In an open-chest pig model, a bolus infusion of 20 mg/kg of N-G-nitro L-arginine methyl ester (L-NAME), a NO synthase i nhibitor, did not alter the regional myocardial perfusion compared with a c ontrol saline injection, as measured by colored microsphares. Using P-31-nu clear magnetic resonance spectroscopy, we showed that the tissue levels of pH and adenosine triphosphate (ATP) but not those of creatine phosphate wer e significantly preserved in the L-NAME group compared with the placebo gro up during the subsequent 15-min regional ischemia. Thus, L-NAME reduced myo cardial ATP utilization during ischemia, and the mechanism underlying these effects is independent of tissue perfusion changes. However, L-NAME did no t accelerate the recovery of ATP levels following reperfusion, suggesting d istinct roles of endogenous NO during reperfusion. (C) 2000 Academic Press.