© 1966 American Heart Association, Inc.
Sympathetic and Parasympathetic Interactions upon the Left Ventricle of the Dog
1 Research Division, St. Vincent Charity Hospital, Department of Physiology, Western Reserve University and the Bio-engineering Group of the Division of Engineering, Case Institute of Technology, Cleveland, Ohio
In canine, isovolumetric, left ventricle preparations, stimulation of the cardiac end of a cut cervical vagus nerve evokes a biphasic change of left ventricular systolic pressure (LVSP). Characteristically, there is a definite reduction of LVSP during the stimulus, followed by a slight increase of LVSP after cessation of stimulation. The magnitude of the reduction of LVSP during vagal stimulation is considerably augmented when sympathetic activity is increased either directly (by electrical stimulation of the left stellate ganglion) or reflexly (by lowering carotid sinus pressure). These results indicate that the effect of vagal stimulation is mediated, at least in part, by antagonizing the positive inotropic influence of the prevailing sympathetic nervous activity. The mechanism of the poststimulation rebound is unknown. It may be due to cardiac sympathetic fibers in the canine vagosympathetic nerve trunks and to the release of catecholamine-like substances in the myocardium.
Key Words: ventricular contractility • vagus nerve fibers • ventricular performance • sympathetic nerve fibers nervous • control of ventricular performance • carotid sinus reflex • anesthetized dogs
Accepted on January 31, 1966
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