Author + information
- Received August 31, 1982
- Revision received January 3, 1983
- Accepted January 5, 1983
- Published online June 1, 1983.
- Ernst A. Raeder, MD,
- Richard L. Verrier, PhD, FACC and
- Bernard Lown, MD, FACC, Professor of Cardiology*
- ↵*Address for reprints: Bernard Lown, MD, Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, Massachusetts 02115.
Beta-adrenergic blocking agents differ considerably in their effects on myocardial excitable properties. The possibility that intrinsic sympathomimetic activity might contribute to such differences has not been adequately explored. This study examined the influence of intrinsic sympathomimetic activity on the electrophysiologic effects of three agents with varying degrees of such activity. Intravenous propranolol (0.5 mg/kg), oxprenolol (0.5 mg/kg) and pindolol (0.05 mg/kg) were administered in 16 anesthetized dogs. The effects of the drugs on ventricular vulnerability were studied over a 2 hour period. Propranolol and oxprenolol raised the ventricular fibrillation threshold by 42 and 56%, respectively. In contrast, pindolol resulted in an elevation of only 25%. After depletion of endogenous norepinephrine stores using reserpine, pindolol led to a decrease of the ventricular fibrillation threshold, which was reversed by propranolol. These data indicate that intrinsic sympathomimetic activity of beta-adrenergic blocking agents substantially alters their ultimate effect on myocardial excitable properties.
This study was supported in part by Grants HL-07776 and HL-28387 from the National Heart, Lung, and Blood Institute, National Institutes of Health, U.S. Public Health Services, Bethesda, Maryland
- Received August 31, 1982.
- Revision received January 3, 1983.
- Accepted January 5, 1983.
- American College of Cardiology Foundation