Cardiac arrhythmias induced by guanethidine in cats anesthetized with halothane

Abstract

Rapid i.v. administration of guanethidine provokes severe and susteined ventricular arrhythmieas in cats anesthetized with halothane. The arrhythmias premature ventricular exciations, multifocal ventricular rhythm, bigeminy, trigeminy and ventricular tachycardia. They begin in about 20 sec and last from 4 to 19 min. By comparison, a standard dose of noradrenaline (10 ωg/kg) induces ventricular arrhythmias which develop in about 12 sec and continue for 1–2.5 min. Pretreatment with β-adrenoceptor blocking drugs prevents arrhythmias from both drugs, and pretreatment with imipramine or reserpine prevents arrhythmias from guanethidine but not noradrenaline. The adrenergic neuron blocking action of guanethidine does not alter the arrhytmogenic action of guanethidine since arrhythmias can still be produced after adrenergic neuron blockade. These results indicate that guanethidine causes arrhythmias by releasing noradrenaline from cardiac adrenergic neuron storage sites and, therefore, point out the vulnerability of the heart to arrhythmias when noradrenaline-releasing drugs interact with halogenated hydrocarbon anesthetics.