The electrophysiological effect of ethacizine, an antiarrhythmic agent of class IC, was studied in dogs with experimental myocardial infarction under the beta-adrenergic stimulation conditions. It was found that ethacizine (i) slows down the atrioventricular conduction and the AV-node conduction; (ii) increases the time of the sinus node function recovery; and (iii) increases the effective atrioventricular refractory periods. Under the conditions of isoproterenol-induced stimulation of the beta-adrenergic structures, some of the ethacizine effects (e.g., increased refractoriness) completely disappeared and the other (slowed down conduction) decreased. As the stimulation frequency was increased, the effect of ethacizine upon the conduction exhibited a decrease. Upon the isoproterenol injection, dependence of the QRS complex on the forced rhythm frequency disappeared.
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