Action of cocaine and chronic sympathetic denervation on vagal escape.
1. The effect of cocaine has been studied on vagal escape and on the tachycardia due to vagal stimulation in the atropinized dog. All the dogs were submitted to acute cervical section of the spinal cord and acute or chronic sympathetic denervation.2. Cocaine, 5 mg/kg or 40 mug/kg/min, I.V., induces a significant enhancement of the ventricular escape. The effects of a continuous infusion of cocaine are more reproducible than those of a single injection of the drug.3. Cocaine, 40 mug/kg/min, I.V., potentiates the tachycardia due to vagal stimulation in the atropinized dog.4. Chronic thoracic sympathectomy markedly retards the recovery of the ventricular rate from the inhibitory action of the vagus. Under this condition, the infusion of cocaine does not significantly enhance the ventricular escape.5. These findings suggest that an adrenergic mechanism located at the sympathetic nerves supplying the heart is substantially involved in the phenomenon of vagal escape.
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D003042:Cocaine / Q000494:pharmacology*; D002818:Cordotomy; D003714:Denervation; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D006321:Heart / Q000294:innervation; D006339:Heart Rate / Q000187:drug effects*; D006352:Heart Ventricles; D008297:Male; D013564:Sympathetic Nervous System / Q000502:physiology*; D013610:Tachycardia / Q000209:etiology; D014630:Vagus Nerve / Q000502:physiology
D001285:Atropine; D003042:Cocaine