Abstract
The possible antiarrhythmic action of prazosin was studied on two experimental models: a focus of ectopic automaticity in the rat isolated right ventricle and arrhythmias induced by i.v. CaCl2 in anaesthetized animals. In vitro, prazosin at 10(-5)M abolished the ectopic automaticity focus in 83% of cases (10/12). The effects of prazosin were not modified by reserpine pretreatment. In vivo, prazosin modified the range of CaCl2 arrhythmias, reduced the mean control sinus rate (by 21.7% at 1 mg/kg), reduced incidence and mortality by ventricular fibrillation and lengthened survival time of animals that eventually died. The results indicate that antagonism of postsynaptic alpha 1-adrenoreceptors may partly explain the efficacy of prazosin against some experimental cardiac arrhythmias.
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