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Adrenergically Mediated Ventricular Fibrillation in Probucol‐Treated Dogs: Roles of Alpha and Beta Adrenergic Receptors

A high incidence of sudden death due to ventricular fibrillation (VF) has been observed in dogs under chronic treatment with probucol, a new hypocholesterolemic agent. The present study describes the cardiac electrophysiologic properties of probucol‐treated dogs and characterizes the electrophysiological response of these animais to manipula‐tion of the autonomic nervous system. There was no significant difference in the spontaneous sinus cycle length, the QT interval, refractory period of the atrium, ventricle or A‐V junction between normal and probucol‐treated dogs. Epinephrine produced VF with few and sometimes no preceding premature ventricular extra‐systoles. Electrical stimulation of the left stellate ganglion induced VF in 16/19 dogs whereas stimulation of the right stellate ganglion induced VF in 1/19 dogs. Phenyl‐ephrine induced VF in 0/19 dogs, isoproterenol in 5/19 dogs, but phenylephrine + isoproterenol induced VF in 9/11 dogs in which isoproterenol did not produce VF. α(phentolaminej or β (propranolol) blockade prevented initiation of VF by epi‐nephrine, phenylephrine + isoproterenol, and left stellate stimulation but a blockade did not prevent induction of VF by isoproterenoJ when isoproterenol alone produced VF. In this nonischemic model, we conclude that left stellate stimulation is a far more potent initiator of VF than right stellate stimulation and that induction of VF appears to require both α and β adrenergic receptor stimulation.