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Increased delivery of free fatty acids raises myocardial oxygen consumption (MVO(2)) without influencing mechanical performance. The effects of norepinephrine on MVO(2) and on the size of ischemic injury after acute coronary occlusion were therefore studied before and during inhibition of lipolysis with beta-pyridylcarbinol. In spite of similar mechanical responses to norepinephrine, MVO(2) increased by 57+/-11% before and significantly less, 31+/-6%, (P &lt; 0.01) during inhibition of lipolysis. After coronary occlusion the ischemic injury associated with norepinephrine infusion, as evidenced by epicardial mapping of S-T segment elevation, was larger before (7.9+/-1.1 mV) than during inhibited lipolysis (2.8+/-0.4 mV; P &lt; 0.005). Average S-T segment elevation associated with norepinephrine infusion during inhibited lipolysis (2.8+/-0.4 mV) was even lower (P &lt; 0.05) than during control occlusion alone, before drug administration (4.4+/-0.7 mV). In conjunction with an antilipolytic agent, norepinephrine was shown to reduce the extent and magnitude of the myocardial ischemic injury produced by acute coronary occlusion; this could be due to an improved balance between myocardial oxygen supply and requirement.

Importance of Free Fatty Acids as a Determinant of Myocardial Oxygen Consumption and Myocardial Ischemic Injury during Norepinephrine Infusion in Dogs