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AJP - Heart and Circulatory Physiology, Vol 258, Issue 5 1470-H1475, Copyright © 1990 by American Physiological Society
ARTICLES |
R. J. Henning, I. R. Khalil and M. N. Levy
Division of Investigative Medicine, Mt. Sinai Medical Center.
We studied the effects of stimulation of the vagal and sympathetic cardiac nerves on left ventricular contraction and relaxation in 16 anesthetized dogs. In each experiment, we paced the ventricles at a fixed rate of 120 beats/min, and we kept the systemic arterial pressure constant. We used the maximum rates of left ventricular pressure rise (dP/dtmax) and fall (dP/dtmin) as our indexes of ventricular contraction and relaxation. Sympathetic nerve stimulation at a frequency of 6 Hz increased dP/dtmax by 802 mmHg/s and raised dP/dtmin by 847 mmHg/s above the control level. The effect of vagal nerve stimulation was directly dependent on the level of sympathetic stimulation. In the absence of sympathetic stimulation, vagal nerve stimulation at a frequency of 5 Hz decreased dP/dtmax by 187 mmHg/s and reduced dP/dtmin by 199 mmHg/s below the control level. When the sympathetic stimulation was 6 Hz, vagal nerve stimulation at 5 Hz decreased dP/dtmax by 513 mmHg/s and reduced dP/dtmin by 709 mmHg/s. Furthermore, propranolol, in doses of 1.5 mg/kg, abolished any significant vagal effect on ventricular contraction or relaxation. We conclude that combined sympathetic-vagal stimulation results in a substantial antagonistic interaction such that vagal stimulation significantly attenuates the sympathetic enhancement of left ventricular function.
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