This study was designed to test the efficacy of glucagon in the treatment of hemodynamic abnormalities of acute and healing experimental canine myocardial infarction. Myocardial infarction was produced in intact, conscious dogs by gradual inflation of a balloon cuff device implanted around the left anterior descending coronary artery 1 to 2 weeks prior to the study. Hemodynamic and metabolic effects of 50 &mgr;g/kg of glucagon were assessed serially in the control state, 1 hour after myocardial infarction and again 1 week later. In the control state glucagon improved cardiac performance and increased myocardial oxygen consumption. One hour after acute myocardial infarction glucagon improved cardiac performance and reduced the degree of left ventricular failure, without any increase in myocardial oxygen consumption. Similar effects of glucagon were noted in the healing phase of myocardial infarction. It is postulated that in this animal model in the presence of heart failure due to myocardial infarction there are reciprocal changes in the factors that increase myocardial oxygen consumption (glucagon-induced inotropy) and decrease oxygen consumption (fall in ventricular end-diastolic volume and wall stress), resulting in no net change in oxygen requirement.