Ventricular tachyarrhythmias associated with digitalis toxicity are believed to be due, in part, to cardiac glycoside-mediated increased central sympathetic neural activity. Because dopaminergic receptor agonists reduce sympathetic outflow, this study assessed effectiveness of the available dopaminergic agonist, bromocriptine, in slowing or terminating ouabain-induced ventricular tachycardia in anesthetized dogs. In all experiments, ouabain was administered intravenously (20 μg/kg body weight bolus injection, followed by 2.5 μg/kg per min infusion) until the onset of stable ventricular tachycardia. Of seven untreated dogs (Group 1), ouabain-induced ventricular tachyarrhythmias resulted in ventricular fibrillation in three, while in four dogs tachycardia persisted without significant change in rate until the study was terminated. Fourteen dogs (Group 2) received bromocriptine, either 30 μg/kg (Group 2A) or 50 μg/kg (Group 2B), after the onset of ventricular tachycardia. Tachycardia slowed in all 14 dogs and terminated with resumption of sinus rhythm in 8 of the 14. In all six dogs pretreated with the peripheral dopaminergic antagonist domperidone (Group 3), bromocriptine, 50 μg/kg, slowed ventricular tachycardia and in three of the six, tachycardia terminated. In contrast, of five dogs pretreated with haloperidol, a central and peripheral dopaminergic receptor antagonist (Group 4), bromocriptine, 50 μg/kg, failed to slow ventricular tachycardia in three, and two of the three developed ventricular fibrillation. In summary, the dopaminergic receptor agonist, bromocriptine, presumably acting at central dopaminergic receptor sites, consistently slowed and in most cases reversed ouabain-induced ventricular tachycardia in a canine model.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of the American College of Cardiology|
|State||Published - 1984|
Bibliographical noteFunding Information:
From the Departments of Medicine, Surgery and Pediatrics, University of Minnesota Medical School, supported in part by a Veterans of Foreign Wars grant-in-aid (Mr. Kao), by a fellowship grant from the American Heart Association, Minnesota Affiliate (Dr. Pritzker), by Grants HL29460 (Dr. Benditt) and HL06097 (Dr. Kriett) from the National Institutes of Health, Bethesda, Maryland, and by a grant-in-aid from Sandoz, study was tigator of the American Heart in part at the 32nd Annual Scientific Session of the American College of Cardiology, 1anuary 30, 1984; revised manuscript received 1une 5, 1984, accepted 1une 15, 1984.