Abstract

In animals whose hearts were made susceptible to cardiac arrhythmias, methoxamine failed to provoke such arrhythmias. The experimental techniques used included cyclopropane or chloroform sensitization, myocardial infarcts and diphtheria toxin myocarditis. Methoxamine, moreover, prevented epinephrine-cyclopropane or epinephrine-chloroform ventricular tachycardia and ventricular fibrillation.

Methoxamine causes slowing of the heart rate and, on overdosage, sinus pauses and brief periods of AV nodal rhythm. At lethal doses of methoxamine, when death occurs from respiratory arrest, cardiac action is still maintained satisfactorily. Methoxamine's pressor effects appear to be due to increased peripheral resistance, and there was no evidence of direct myocardial stimulation.