Effect of autonomic neural blockade on verapamil-induced suppression of the accelerated ventricular escape beat in ouabain-treated dogs.
The effect of autonomic neural blockade on verapamil-induced suppression of the accelerated ventricular escape beat (AVE) was evaluated in anesthetized dogs pretreated with ouabain. Ouabain (53 +/- 2 microgram/kg, n = 45) was administered in divided doses until simultaneous electrical stimulation of the right atrium and ventricle triggered an AVE. The escape interval of the AVE was stable over a 150-min time period in a group of control animals. Verapamil was infused (20 microgram/kg/min) until the escape interval increased at least 50% or until the AVE was abolished. The total amount of verapamil in milligrams per kilogram that produced this effect was defined as the verapamil endpoint. The verapamil endpoint in vagotomized animals was not significantly different from a group of intact controls. In contrast, the verapamil endpoint in animals pretreated with propranolol, hexamethonium, guanethidine, bretylium or spinal section was significantly less than the control group. Propranolol, hexamethonium, guanethidine or spinal section alone increased the escape interval by a maximum of 12%. Infusion of norepinephrine in spinal animals treated with verapamil restored the AVE. These data indicate that sympathetic nerve activity contributes to the genesis of the AVE and antagonizes the antiarrhythmic effect of verapamil on the escape beat.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced; D001341:Autonomic Nervous System / Q000187:drug effects*; D004285:Dogs; D005260:Female; D006339:Heart Rate / Q000187:drug effects*; D008297:Male; D010042:Ouabain / Q000494:pharmacology*; D013997:Time Factors; D014628:Vagotomy; D014700:Verapamil / Q000494:pharmacology*
D010042:Ouabain; D014700:Verapamil