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. During trigger activity, the extrasystoles were associated with complexes of basic rhythm and transformed themselves into torsades de pointes and ventricular fibrillation.
Moroz
V M
VM
Vinnitsa National University of Medicine.
Lipnitskii
T N
TN
D000255:Adenosine Triphosphate / Q000737:chemistry; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D001145:Arrhythmias, Cardiac / Q000473:pathology / Q000503:physiopathology*; D004562:Electrocardiography; D005260:Female; D007473:Ion Channels / Q000737:chemistry; D007477:Ions; D008297:Male; D051381:Rats; D013610:Tachycardia / Q000378:metabolism; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000473:pathology / Q000503:physiopathology*
D000889:Anti-Arrhythmia Agents; D007473:Ion Channels; D007477:Ions; D000255:Adenosine Triphosphate