[Electrophysiological action of ethacizin in acute myocardial ischemia in dogs].
The effects of ethacizin on delayed activation of the ischemic myocardium by acute left anterior descending coronary artery occlusion were studied in dogs. Ethacizin, administered intravenously at a dose of 0.5 or 1 mg/kg depressed the conduction of excitation in the ischemic myocardium and significantly increased the incidence of ventricular fibrillation. Electrophysiological effects of ethacizin in acute myocardial ischemia, as well as its antiarrhythmic activity at the advanced stages of experimental myocardial infarction might be related to an intensive influence of ethacizin on fast inward sodium current in the myocardial fibers.
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D003327:Coronary Disease / Q000188:drug therapy* / Q000503:physiopathology; D004285:Dogs; D004562:Electrocardiography; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D016293:Moricizine / Q000031:analogs & derivatives*; D010640:Phenothiazines / Q000494:pharmacology*
D000889:Anti-Arrhythmia Agents; D010640:Phenothiazines; C027240:diethylamino-ethmozine; D016293:Moricizine
Elektrofiziologicheskoe deĭstvie étatsizina pri ostroĭ ishemii miokarda u sobak.