Study of pathogenesis of ventricular arrhythmia in experimental rats by separation of sinus and ventricular substitutional rhythms.

Pathogenesis of cardiac arrhythmia was determined by EEC changes after ATP-induced complete atrioventricular block. The re-entry mechanism underlays extrasystoles with equal coupling intervals with complexes of ventricular substitution rhythms, which transformed into paroxysmal tachycardia with equal R-R intervals, ventricular flutter, and ventricular fibrillation. Ectopic automaticity was characterized by extrasystole unrelated to the complexes of substitutional rhythms, which was transformed into accelerated idioventricular rhythm and asystole.

Dysfunction of ionic channels in cardiomyocyte sarcolemma and cardiac arrhythmias.

The arrhythmic effects of Na+ and Ca2+ intracellular imbalance were examined on rats with aconitine-induced cardiac arrhythmias. Under conditions of Na(+)-dependent arrhythmogenesis, blockade of Ca(2+)-channels with verapamil aggravated cardiac rhythm disturbances. Correction of ionic imbalance by intravenous injection of calcium preparations in aconitine-induced arrhythmia promoted recovery of stable sinus rhythm and decreased animal mortality.