Electrophysiologic effects of new ester of ajmaline 17-monochloroacetyl ajmaline hydrochloride (MCAA).
A new ajmaline ester, 17-monochloroacetyl ajmaline hydrochloride (MCAA) which has shown important clinical antiarrhythmic effects was studied in 20 isolated perfused rabbit hearts. Transmembrane potentials were recorded in atrial ventricular and A-V junctional fibers before and after perfusion of 3 mg/l of MCAA. There was a significant decrease in the action potential amplitude (81.1 plus or minus 6.0 to 75.2 plus or minus 5.8mV) overshoot (23.1 plus or minus 5.9 to 16.1 plus or minus 2.9mV) and maximum rate of depolarization (63.4 plus or minus 30.8 to 40.7 plus or minus 19.7 V/sec) and an increase in the action potential duration (119.8 plus or minus 12.6 to 135.6 plus or minus 25.1 msec). The strength interval curve was shifted to the right by MCAA. Conduction was increased in the atria and AV junction but not in the His-Purkinje system. MCAA appears to be a quinidine-like agent except for His-Purkinje conduction. This agent could offer important antiarrhythmic effects in atrial and ventricular arrhythmias.
D000200:Action Potentials; D000404:Ajmaline / Q000494:pharmacology*; D000818:Animals; D016275:Atrial Function; D004594:Electrophysiology; D004952:Esters; D006321:Heart / Q000187:drug effects*; D006329:Heart Conduction System; D008564:Membrane Potentials; D010477:Perfusion; D011689:Purkinje Cells / Q000502:physiology; D011802:Quinidine / Q000494:pharmacology; D011817:Rabbits
D004952:Esters; D000404:Ajmaline; D011802:Quinidine