Effects of Antiarrhythmic Agents and Mg²⁺ on Aconitine-induced Arrhythmias

Abstract

The effects of antiarrhythmic agents, including Classes I and IV and 3-10mM Mg²⁺ on aconitine-induced arrhythmias were examined using a conventional microelectrode and patch clamp method in Langendorff-perfused rabbit hearts and isolated guinea-pig ventricular myocytes. Intracoronary application of 0.1μM aconitine induced polymorphic ventricular tachycardia (PVT) which continued for more than 60 minutes. Application of aconitine to ventricular myocytes caused a prolonged action potential duration (APD) and the appearance of early afterdepolarization (EAD) together with the occurrence of an inward hump of the I-V curve around -60 to -40mV and increased outward current at positive voltages. Application of 10μM TTX and 5mM or higher Mg²⁺ restored aconitine-induced PVT to sinus rhythm in Langendorffperfused preparations and also shortened the prolonged APD, demonstrating the abolishment of EAD by aconitine in ventricular myocytes. However, antiarrhythmic agents did not exert such effects. In conclusion, the antiarrhythmic actions of Mg²⁺ and TTX in aconitine-induced arrhythmia are to abolish EAD and shorten the prolonged APD by suppression of the inward Na⁺ current around -60 to -40mV.