Ventricular arrhythmias in cardiac anaphylaxis

Abstract

Arrhythmogenic effects of anaphylaxis and histamine were studied in guinea pigs by measuring changes of transmembrane potentials from isolated papillary muscles. Antigenic challenge of preparations obtained from passively sensitized animals induced ventricular automaticity in 1/3 of the experiments. The arrhythmogenic effects of cardiac anaphylaxis could be reproduced by exogenous histamine. Abnormal automaticity was associated with a stable diastolic membrane potential in most of the ventricular fibres and only occasionally ectopic pacemaker potentials were observed in fibres near the ventricular septum. The effective refractory period, maximum rate of depolarization of the action potential and electrical threshold were not significantly changed in ventricular anaphylaxis but in the presence of histamine the refractory time was shortened. Ventricular arrhythmias induced by histamine were increased at high extracellular Ca2+ concentrations and inhibited by Mn2+ and D 600 but were only moderately antagonized by tetrodotoxin. Pretreatment with reserpine had no effect on the abnormal automaticity. Spontaneous ventricular activity caused by histamine was markedly inhibited by the histamine H2-receptor antagonist burimamide and also by the antiarrhythmic drug, prajmalium bitartrate. The H1-receptor antagonist brompheniramine, hydrocortisone and propranolol had little or no antiarrhythmic effect.