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AJP - Heart and Circulatory Physiology, Vol 259, Issue 5 1365-H1373, Copyright © 1990 by American Physiological Society
ARTICLES |
C. K. Butler, F. M. Smith, R. Cardinal, D. A. Murphy, D. A. Hopkins and J. A. Armour
Department of Surgery, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.
The purpose of the present study was to examine cardiac effects induced by electrical stimulation (1-4 V, 1 ms, 200 Hz) of discrete loci within the ganglionated plexi located on canine atria and ventricles. When 20 loci in the right atrial ventral ganglionated plexi of 11 anesthetized open-chest dogs were stimulated, bradycardia and/or right and left atrial force suppression occurred when, on average, 15% of these loci were stimulated. Bradycardia and atrial force suppression were elicited when, on average, 8% of 15 loci in the left atrial ventral ganglionated plexi of eight dogs was stimulated. When these loci were restimulated after acute decentralization, cardiac responses were attenuated or occasionally eliminated. After atropine (1 mg/kg iv) administration, repeat stimulation of loci in the right but not left atrial ganglionated plexus induced tachycardia. Stimulation of loci in the right ventricular ganglionated plexus after the subsequent administration of desipramine (1 mg/kg iv) in six dogs resulted in an increase in right ventricular conus intramyocardial pressure. After hexamethonium administration (10 mg/kg iv, followed by a continuous infusion of 1 mg.kg-1.min-1), sympathetic responses were no longer elicited from one of the five dogs in which loci in the right atrial ganglionated plexi and from two of the six dogs in which loci of the right ventricular ganglionated plexus had elicited responses. We conclude that atrial and ventricular ganglionated plexi contain efferent parasympathetic, efferent sympathetic, and afferent neurons.
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