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  • 1 Institute of Medical Physiology, School of Medicine, University of Belgrade Višegradska 26, 11000 Belgrade, Serbia and Montenegro
  • 2 Institute of Medical Physiology, School of Medicine, University of Belgrade Višegradska 26, 11000 Belgrade, Serbia and Montenegro
  • 3 Institute of Medical Physiology, School of Medicine, University of Belgrade Višegradska 26, 11000 Belgrade, Serbia and Montenegro
  • 4 Institute of Medical Physiology, School of Medicine, University of Belgrade Višegradska 26, 11000 Belgrade, Serbia and Montenegro
  • 5 Institute of Medical Physiology, School of Medicine, University of Belgrade Višegradska 26, 11000 Belgrade, Serbia and Montenegro
  • 6 Institute of Medical Physiology, School of Medicine, University of Belgrade Višegradska 26, 11000 Belgrade, Serbia and Montenegro
  • 7 Institute of Anesthesiology, Emergency Center, School of Medicine, University of Belgrade Serbia and Montenegro
  • 8 Institute of Anesthesiology, Emergency Center, School of Medicine, University of Belgrade Serbia and Montenegro
  • 9 Institute of Anesthesiology, Emergency Center, School of Medicine, University of Belgrade Serbia and Montenegro
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In our previous work we have shown that in mouse heart basal level of endothelial produced nitrite, as a marker of nitric oxide (NO) formation, was 9.7 nmol l-1. Bradykinin (10 mmol l-1) induced a 5-fold rise in nitrite release, the coronary venous effluent concentration being 58 nmol l-1, but there was no effect on myocardial oxygen consumption (MVO2). The aim of this study was to assess the levels of authentic nitric oxide solution, exogenously applied, on myocardial oxygen consumption. Isolated mouse hearts (n=36) were paced (500 imp./min) and perfused at constant flow (16.0±0.3 ml g-1 min-1). When coronary vasculature resistance was carefully controlled by adenosine (1 mmol l-1), authentic nitric oxide solution, in a concentration less than 5 mmol l-1 did not alter myocardial oxygen consumption. Only concentrations of nitric oxide higher than 5 mmol l-1 induced reduction in myocardial oxygen consumption. Thus in the saline perfused mouse heart, with carefully controlled vasodilatation, modulating myocardial nitric oxide levels using an arterial application of authentic nitric oxide, concentrations higher than 5 mmol l-1 of nitric oxide were required to induce a decrease in myocardial oxygen consumption.

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