Abstract
While the increase in cardiac work, force and rate are known to be a function of beta-adrenergic receptor stimulation, the mechanism of metabolic actions is uncertain. This study was undertaken to clarify the “calorigenic” action of epinephrine and its relation to hemodynamic changes. In a group of canine heart-lung preparations, the intra-atrial infusion of 0.01, 0.03 and 0.1 μg/kg of epinephrine did not change the cardiac work, force and rate, of the myocardial oxygen consumption, as compared to the control. However, intra-atrial infusion of 0.5 μg/kg of epinephrine caused an increase in cardiac work, cardiac isometric contraction, coronary flow and a marked elevation in the myocardial oxygen consumption above and beyond the rate of its effect on the cardiac hemodynamic parameters. Addition of 0.5 mg/kg of Sotalol did not cause depression of these parameters of left ventricular functions, including the coronary flow. However, 0.5 mg/kg of Sotalol effectively blocked the “calorigenic” action of 0.5 μg/kg of epinephrine. Apparently, more oxygen is being extracted by the myocardium after 0.5 μg/kg of epinephrine. Sotalol blocks this calorigenic action of epinephrine. Since the metabolic effects of epinephrine have not been shown to be beta-adrenergic receptor-mediated changes, it is concluded that Sotalol has the unique property of blocking the metabolic action of epinephrine.
