The effect of a benzotriazinium salt on in vitro and in vivo arrhythmias in guinea-pigs and mice.

In guinea-pig Langendorff hearts, a benzotriazinium derivative, 2-n-propyl-4-p-tolylamino-1,2,3-benzotriazinium iodide (TnPBI), increased the ventricular refractory period, increased the ventricular fibrillation threshold to electrical stimulation and converted persistent ventricular fibrillation to sinus rhythm. TnPBI also converted aconitine-induced tachyarrhythmias to sinus rhythm in the same preparation. In mice pretreated with TnPBI, both acutely and chronically, the amount of intravenous aconitine necessary to produce cardiac arrhythmias was increased. In guinea-pigs anaesthetised with halothane. TnPBI converted adrenaline-induced arrhythmias to sinus rhythm.