Glucagon: its enhancement of atrioventricular nodal pacemaker activity and failure to increase ventricular automaticity in dogs.

The effects of glucagon on atrioventricular nodal automaticity and ventricular automaticity were studied in anesthetized open-chest dogs. After the sinoatrial node was crushed, glucagon, 4 fig/kg, produced a marked and sustained increase in the rate of A-V nodal discharge (27.6 ± 10.1 vs. 117.4 ± 6.5 beats/min) that persisted for an average of 20 minutes. The effect of glucagon was not modified by previous administration of propranolol, 2 mg/kg. Repeated administrations of glucagon, 1 /u.g/kg every 15 min, for a period of 2 hours, sustained A-V nodal rhythm. The effects of glucagon on ventricular automaticity were'studied in unanesthetized dogs 48 and 72 hours after surgical ligation of the anterior descending coronary artery and were compared to the effects of epinephrine. Unlike the catecholamine, glucagon did not enhance ventricular automaticity in the infarcted myocardium. The results suggest that glucagon might be of therapeutic value in the management of heart block and in cardiogenic shock after acute myocardial infarction. The inability to augment ventricular ectopic activity suggests that glucagon possesses an advantage over the catecholamines as an inotropic agent. ADDITIONAL