Effect of fentanyl on myocardial metabolism during ischemia

In this survey, the effect of fentanyl, a potent morphinomimetic, on myocardial metabolism and some hemodynamic variables during ischemia is described. The data presented were derived from open-chest experiments on dogs. Ischemia was induced by partial occlusion (stenosis) of a coronary artery. Inducing the stenosis twice in the same animal after a certain interval made it possible to use the animal as its own control. Control and compound series are discussed. In the compound series, fentanyl (25 microgram/kg-1) was injected IV 5 minutes before induction of the second stenosis. Fentanyl decreased the oxygen demand of the ischemic myocardium, mainly due to a reduction in heart rate, which resulted in a decrease in the breakdown of energy-rich phosphates and in the anaerobic breakdown of glucose. The latter resulted in a less pronounced production of lactate by the ischemic myocardium and hence in a diminished acidity of this tissue. The release of potassium ions during ischemia was reduced after fentanyl. The uptake of glucose by the ischemic myocardium was not affected by fentanyl, but the uptake of free fatty acids was diminished. During ischemia, the arterial free fatty acid concentration decreased after fentanyl, indicating that the compound may suppress stress responses. Although extrapolation to clinical anesthesia should be handled with care, the described findings suggest that the use of fentanyl may benefit patients with coronary artery disease during anesthesia.