Effects of atropine on the cardiac arrest induced by propranolol and digitoxin in dogs.
The present study examines the hypothesis that vagal activity can accelerate the onset of cardiac arrest produced by administering a beta-adrenergic blocking dose of propranolol to digitoxin-intoxicated dogs. In 11 experiments, intravenous injection of 0.75 mg/kg propranolol into digitoxin intoxicated dogs induced a sustained ventricular asystole (early-phase cardiac arrest). In six of these eleven experiments, intermittent pacing of the ventricles for as long as 150 min to maintain blood pressure after the onset of asystole, led to the resumption of spontaneous heart beats in only one dog. In five other experiments, injection of atropine (1 mg/kg) three min after the onset of early-phase cardiac arrest elicited sustained spontaneous junctional rhythms. In another four experiments the injection of atropine prior to or simultaneously with propranolol prevented the occurrence of asystole and caused the emergence of a junctional pacemaker. In eight experiments in which the cardiac arrest was reversed or prevented, injection of maintenance doses of atropine and propranolol caused eventual failure of the junctional pacemaker (late-phase cardiac arrest). This failure could not be prevented or reversed by atropine. The results suggest that early-phase cardiac arrest is due to vagal suppression of cardiac pacemakers and therefore supports the above hypothesis.
D000818:Animals; D001285:Atropine / Q000494:pharmacology*; D004074:Digitoxin; D004285:Dogs; D004562:Electrocardiography; D005260:Female; D006321:Heart / Q000503:physiopathology; D006323:Heart Arrest / Q000139:chemically induced / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D011433:Propranolol
D001285:Atropine; D011433:Propranolol; D004074:Digitoxin