Cardiovascular effects of nicotine in the conscious dog: Modification by changes in autonomic tone

Abstract

Studies were performed in conscious dogs in which catheters had previously been positioned for long-term use in the right atrium, right ventricle, pulmonary artery and central aorta. Doses of less than 200 μ g of nicotine injected into the right atrium produced no significant hemodynamic effects. A dose of 200 μ g of nicotine produced initial tachycardia, a subsequent hypertensive response and reflex bradycardia. A 400 μ g dose of nicotine produced a triphasic response: (1) a 2 to 4 second sinus arrest, (2) subsequent sinus tachycardia and marked hypertensive response, and (3) reflex bradycardia with persistent increases in right ventricular end-diastolic pressure. Arterial administration of nicotine in similar doses produced only hypertension and reflex bradycardia. No asystole or tachycardia was observed. Pretreatment with atropine eliminated the asystole produced by intravenous administration of nicotine but did not alter the reflex tachycardia occurring after intravenous or intraarterial administration of nicotine. Pretreatment with propranolol did not prolong the asystole occurring after intravenous administration of nicotine and did not diminish the peak increase in heart rate during phase 2. However, the reflex bradycardia was more pronounced after nicotine was given either intravenously or intraarterially. We conclude that, in the conscious dog, nicotine (1) releases acetylcholine in the right atrium, (2) may depress myocardial function, and (3) produces significant hypertension and reflex bradycardia.