Abstract

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.