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Institut für Pathophysiologie, Zentrum für Innere Medizin des Universitätsklinikums Essen, 45147 Essen, Germany
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) toward carbohydrate utilization. Ischemic myocardium is
characterized by a similar shift toward preferential carbohydrate
utilization, although NO synthesis is increased. The importance of NO
for myocardial metabolism during ischemia has not been analyzed
in detail. We therefore assessed the influence of NO synthase
inhibition with NG-nitro-L-arginine
(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. Before ischemia, L-NNA
decreased myocardial FFA consumption (M
FFA;
P < 0.05), while consumption of carbohydrate and
O2 (MO2) remained
constant. ATP equivalents [calculated with the assumption of 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
MFFA, while MO2
increased (P < 0.05) and ATPeq and
regional myocardial function remained constant. During
ischemia, alterations in myocardial metabolism were similar in
control and L-NNA-treated animals: MFFA
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.
nitric oxide; free fatty acids; glucose; lactate; myocardial ischemia
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