Cocaine depresses cardiac sympathetic efferent activity in anesthetized dogs

Increased use of cocaine has increased the incidence of sudden cardiac death concomitantly, likely due to life-threatening arrhythmias and/or myocardial ischemia. The effects of cocaine on regulation of the heart and circulation by the autonomic nervous system (which is active during arrhythmias and myocardial ischemia) are not fully understood, however. Therefore, we wished to evaluate the influence of intravenous (i.v.) cocaine on spontaneous thoracic cardiac sympathetic efferent nerve activity in anesthetized dogs. In six pentobarbital-anesthetized dogs, blood pressure (BP), heart rate (HR), and two cardiac sympathetic nerves (6 right-sided, 6 left-sided; 3 preganglionic, 9 postganglionic) were simultaneously recorded. Cocaine was infused for 15 min to a total dose of 6 mg/kg. Sympathetic multifiber efferent activities, HR, and BP were recorded continuously throughout the infusion and quantified at 5-min intervals during the infusion and for 45 min after infusion. Neural activities declined sharply to 54.7% of control (p less than 0.01) after only 5 min of infusion. After 15 min of infusion, nerve activity decreased to 39.4% of control (p less than 0.01). Cardiac nerve activity remained depressed (44.9%; p less than 0.01) 45 min after cocaine infusion. Cocaine caused a slight decrease in both HR and BP at 15 min. The rate-pressure product (RPP) decreased significantly during cocaine infusion. Comparable administration of lidocaine (6 mg/kg i.v. in 15 min) failed to influence cardiac sympathetic efferent activities significantly. We conclude that i.v. cocaine significantly depresses spontaneous cardiac sympathetic efferent neural activities in anesthetized dogs.