Effects of glucagon on myocardial contractility and hemodynamics in acute experimental myocardial infarction. Basis for its possible use in cardiogenic shock

Abstract

Effects of glucagon administered intravenously either as a bolus or as an infusion were investigated in dogs with acute myocardial infarction. Glucagon was found to augment the contractile state of the noninfarcted portion of the left ventricle, as indicated by an upward shift of the forcevelocity relation. Left ventricular performance as estimated from the relation between left ventricular end-diastolic pressure and left ventricular minute work fell after myocardial infarction. In a similar manner, the left ventricular contractility, as defined by the rate of left ventricular pressure rise from a given level of left ventricular end-diastolic pressure, also showed a decline after myocardial infarction. Glucagon reversed these changes: It resulted in a lowering of left ventricular end-diastolic pressure and an increase in left ventricular work and the rate of left ventricular pressure rise. Cardiac output, which fell after infarction, rose after glucagon. Glucagon resulted in a rise in the mean arterial pressure from the lowered values which prevailed after infarction. The peripheral vascular resistance varied after infarction. After glucagon, there was a uniform decline in peripheral resistance. While an increase in the heart rate as a manifestation of the positive chronotropic effect of glucagon was marked, absence of cardiac arrhythmias was noteworthy. These effects of glucagon point to its potential therapeutic value in the treatment of the circulatory and/or myocardial failure which may accompany an acute myocardial infarction.