Effect of Enhanced Contractility on the Left Ventricular Response to Vagus Nerve Stimulation in Dogs
In the canine isovolumetric left ventricle preparation, stimuli were applied to the efferent end of a transected cervical vagus nerve. The changes in left ventricular systolic pressure in response to vagal stimulation were compared under control conditions and when ventricular contractility was enhanced by various kinds of inotropic stimulation-left stellate ganglion stimulation, paired pacing, calcium chloride infusions, aminophylline infusions, and acetylstrophanthidin injections. Vagal stimulation under control conditions caused mean decreases in pressure in the various groups ranging from 13.2 to 16.2% of the control level. The depressant effect of vagal stimulation was potentiated during sympathetic stimulation, in confirmation of previous findings; the mean decrease in pressure produced by vagal stimulation during concurrent sympathetic stimulation varied from 20.1 to 20.8%. Calcium and aminophylline infusions had no significant effect on the ventricular response to vagal stimulation; the percent reductions in pressure caused by vagal stimulation were 18.1 and 15.5%, respectively. However, the response to vagal stimulation was markedly attenuated during paired pacing and after acetylstrophanthidin; the percent reductions in pressure caused by vagal stimulation were 5.0 and 9.4%, respectively. The potentiation of the response to vagal stimulation during increased cardiac sympathetic activity probably represents a specific adrenergic-cholinergic interaction.
- autonomic nervous system
- inotropic stimuli
- sympathetic-parasympathetic interaction
- cardiotonic agents
- adrenergic-cholinergic interaction
- paired pacing
- cardiac glycosides
- Received October 7, 1968.
- Accepted January 3, 1969.
- © 1969 American Heart Association, Inc.