Abstract
Several groups of drugs have been shown to possess antiarrhythmic activity. Some of them e.g. quinidine, procainamide, local anaesthetics, β-receptor blocking agents and diphenylhydantoin etc. have achieved a clinical status as antiarrhythmic drugs. Diphenylhydantoin (dilantin) an anticonvulsant has been successfully employed for the supression of ventricular arrhythmias due to digitalis over dosage (1) and anaesthesia (2). Atrial arrhythmias on the other hand, did not respond to diphenylhydantoin therapy. Other anticonvulsants like trimethadione (Tridione) and paramethadione (Paradione) have not been studied for the antiarrhythmic activity. Though there is enough clinical evidence of cardiac arrhythmias of central origin viz. arrhythmias during hypothalamic operation (3) electroconvulsive therapy (4) and second stage of anaesthesia, yet in the screening of antiarrhythmic activity most of the workers have neglected the arrhythmias of central nervous system origin. We have recently reported that aconitine induced centr ogenic arrhythmia is a good model for screening of antiarrhythmic agents (5). Moreover for the screening of antiarrhythmic activity of CNS active agents, it seems logical that one must include some model of centrogenic arrhythmia as well. In the present investigation diphenylhydantoin, trimethadione and paramethadione have been studied against four types of experimental cardiac arrhythmia viz. (I) aconitine induced centrogenic ventricular arrhythmias (II) aconitine induced auricular arrhythmias (III) hydrocarbon-epinephrine induced ventricular arrhythmias (IV) and coronary-ligation induced ventricular arrhythmias.
