[Electrophysiological effects of ethacizine in experimental myocardial infarction and stimulation of sympathetic heart innervation].
The electrophysiological effect of ethacizine, an antiarrhythmic agent of class IC, was studied in dogs with experimental myocardial infarction under the beta-adrenergic stimulation conditions. It was found that ethacizine (i) slows down the atrioventricular conduction and the AV-node conduction; (ii) increases the time of the sinus node function recovery; and (iii) increases the effective atrioventricular refractory periods. Under the conditions of isoproterenol-induced stimulation of the beta-adrenergic structures, some of the ethacizine effects (e.g., increased refractoriness) completely disappeared and the other (slowed down conduction) decreased. As the stimulation frequency was increased, the effect of ethacizine upon the conduction exhibited a decrease. Upon the isoproterenol injection, dependence of the QRS complex on the forced rhythm frequency disappeared.
Kaverina
N V
NV
Laboratory of Circulation System Pharmacology, Institute of Pharmacology, Russian Academy of Medical Sciences, Baltiiskaya ul. 8, Moscow, 125315 Russia.
Lyskovtsev
V V
VV
Popova
E P
EP
D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D002036:Bundle of His / Q000187:drug effects / Q000503:physiopathology; D004285:Dogs; D004558:Electric Stimulation; D004562:Electrocardiography / Q000187:drug effects; D006321:Heart / Q000294:innervation*; D006339:Heart Rate / Q000187:drug effects; D007545:Isoproterenol / Q000494:pharmacology; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology*; D010640:Phenothiazines / Q000494:pharmacology*; D011943:Receptors, Adrenergic, beta / Q000502:physiology*
D000318:Adrenergic beta-Agonists; D000889:Anti-Arrhythmia Agents; D010640:Phenothiazines; D011943:Receptors, Adrenergic, beta; C046818:ethacizine; D007545:Isoproterenol