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1 Departments of Pharmacology and Thoracic Surgery, University of Michigan Medical School, Ann Arbor, Michigan
Glucagon has been shown to exert a positive inotropic effect in patients with normal cardiac function as well as in patients with mild impairment of cardiac function. In the presence of chronic heart failure, however, the beneficial effects of treatment with glucagon have been somewhat less consistent. Previous in vitro studies had provided evidence to show that papillary muscles obtained from cats with chronic heart failure had lost their ability to develop a positive inotropic response to glucagon. Since it is difficult to apply in vitro papillary muscle data to the intact heart, studies were done to assess the effects of glucagon in the intact cat heart four months after the experimental induction of chronic heart failure due to surgical banding of the pulmonary artery. The cardiohemodynamic effects of glucagon were examined in 12 anesthetized cats (six normal, six with chronic heart failure). At the peak of the dose-response curve, glucagon significantly increased isometric left ventricular force (45.5%), right ventricular pressure (74.8%), right ventricular dP/dt (180%), cardiac output (14%), stroke volume (30%) and cardiac index (14%) in each of the six cats with chronic heart failure. The six normal cats likewise developed a positive inotropic response to the intravenous administration of glucagon. The heart rate in each of the groups was not altered significantly by glucagon. Thus, the augmentation in cardiac output was the result of an increase in stroke volume due to an augmentation of contractile force. Therefore, in contrast to previously reported in vitro observations, glucagon augments myocardial contractility in the intact cat heart in chronic failure.
Submitted on May 21, 1973