The effect of moderate doses of fentanyl (25 μg/kg IV) on free fatty acid metabolism and oxygen utilization of ischemic myocardium and on the release of substances associated with ischemic damage of this tissue, e.g., potassium and hydrogen ions, was studied in anesthetized dogs. The influence of this potent morphinomimetic on left ventricular hemodynamics, glycolysis, and phosphate release during myocardial ischemia was investigated as well. Myocardial ischemia was induced by partial occlusion of the left interventricular artery. Fentanyl diminished the energy demand of the ischemic myocardium, mainly by decreasing heart rate, resulting in a decrease in lactate production and less pronounced release of potassium and hydrogen tons by this tissue. After the administration of fentanyl, arterial free fatty acid concentration decreased resulting in a diminished arteriolocal venous difference of this substrate across the ischemic myocardium. Since the arteriolocal venous differences of glucose during ischemia remained unchanged by fentanyl, carbohydrate metabolism rather than conversion of lipid material became relatively more important for the ischemic myocardium. Utilization of oxygen by the ischemic tissue remained virtually unaffected by fentanyl. Although the present results should be extrapolated to the clinical situation with care, our observations suggest that use of fentanyl may benefit patients with myocardial ischemia during anesthesia. In such patients the diminished energy demand of the ischemic myocardium and the resulting decrease in acidity and reduced release of potassium and utilization of free fatty acids, as well as the possibility to suppress stress responses may protect the jeopardized myocardial tissue against further damage. These beneficial effects may also be observed after the administration of other compounds that decrease heart rate and arterial blood pressure and hence the oxygen demand of the myocardium.
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Vusse et al. (1980) studied this question.