THE EFFECTS OF 6-HYDROXYDOPAMINE ON VAGAL CARDIOACCELERATOR SYSTEMS

¹ Department of Physiology, School of Medicine, University of New Mexico Albuquerque, New Mexico

This study was undertaken to examine the presensce of vagal cardioaccelerator systems in the dog after chemical sympathectomy. Five dogs were pretreated with 50 mg/kg of 6-hydroxydopamine (6-OHDA). Untreated dogs served as controls. Electrical stimulation of the peripheral end of the right vagosympathetic trunk elicited a marked bradycardia in both groups of dogs. After cessation of stimulation, a postvagal tachycardia was observed. There was no significant difference between the magnitude of postvagal tachycardia in the untreated and 6-OHDA-treated dogs. Cardioacceleration was also elicitd by stimulation of the vagosympathetic trunk in atropine-treated dogs and the response was designated as a vagally induced tachycardia (VIT). The magnitude of the VIT from both control and 6-OHDA-treated dogs was not significantly different. Bretylium (5.0 mg/kg) abolished the short latency, fast rate of rise characteristies of the VIT ("fast" component) in the untreated dogs and unmasked a long lateney, slow rate of rise response of the VIT ("slow" component) similar to that observed in the 6-OHDA-treated dogs. Bretylium had no effect on the VIT in the 6-OHDA-treated dogs. It was concluded that the fast component of VIT was due to cardiac sympathetic fibers present in the cervical vagosympathetic trunk. The existence of a slow component of VIT in 6-OHDA-treated dogs is consistent with the hypothesis that vagal fibers activate the release of catecholamines from intracardiac chromaffin tissue.