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* To whom correspondence should be addressed. E-mail: gerd.heusch{at}uni-esen.de.
Nitric oxide (NO) is involved in the control of myocardial metabolism. In normoperfused myocardium, NO synthase inhibition shifts myocardial metabolism from free fatty acid (FFA) towards carbohydrate utilization. Ischemic myocardium is characterized by a similar shift towards preferential carbohydrate utilization, although NO synthesis is increased. The importance of NO for myocardial metabolism during ischemia has not been analyzed in detail yet. We therefore assessed the influence of NO synthase inhibition with L-NG-nitroarginine (L-NNA) on myocardial metabolism during moderate ischemia in anesthetized pigs. In control animals, the increase in left ventricular pressure with L-NNA was mimicked by aortic constriction. Prior to ischemia, L-NNA decreased myocardial FFA consumption (MVFFA) (p<0.05), while carbohydrate and oxygen (MVO2) consumptions remained constant. ATP equivalents - calculated assuming complete oxidative substrate decomposition (ATPeq) - decreased with L-NNA (p<0.05), associated with a decrease of regional myocardial function (p<0.05). In contrast, aortic constriction had no effect on MVFFA, while MVO2 increased (p<0.05) and ATPeq and regional myocardial function remained constant. During ischemia, the alterations in myocardial metabolism were similar in control and L-NNA animals: MVFFA decreased (p<0.05) and net lactate consumption was reversed to net lactate production (p<0.05). Regional myocardial function was decreased (p<0.05), although more markedly in animals receiving L-NNA (p<0.05). We conclude that the efficiency of oxidative metabolism was impaired by L-NNA per se, paralleled by impaired regional myocardial function. During ischemia, L-NNA had no effect on myocardial substrate consumption, indicating that NO synthases were no longer effectively involved in the control of myocardial metabolism.
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