INFLUENCE OF ATRIAL ELECTRICAL STIMULATION ON THE TRANSMURAL SEQUENCE OF DEPOLARIZATION OF VENTRICULAR WALLS IN RAT HEART UNDER ZOLETHYL-XYLAZINE ANESTHESIA

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The transmural sequence of depolarization of the free walls of the ventricles of the heart of Wistar rats was studied with an increase in the heart rate under zoletyl- xylazine anesthesia. The increase in heart rate was caused by atrial electrical stimulation. Zoletyl-xylazine anesthesia with intramuscular injection at a dose of 0.15 mg/kg of zoletil and 3 mg/kg of xylazine caused a significant negative chronotropic effect with pronounced bradycardia, characterized by a decrease in heart rate from the initial two times. With a reduced sinoatrial rhythm with a frequency of 237 ± 34 beats/min, the subendocardial layers were initially depolarized, then the intramural and further subepicardial layers of the left and right free walls of the ventricles of the heart. The areas of the bases of the free walls of the ventricles depolarized later than the apical areas by approximately 2–4 ms, also by the movement of the activation wave from the endocardium to the epicardium. With an increase in heart rate, the sequence and transmural depolarization gradient did not change. At the same time, an increase in the stimulation frequency from 300 to 500 beats/min led to a decrease in the time of arrival of the depolarization wave to the subendocardial, intramural, and subepicardial layers of the walls of the left and right ventricles. Despite the depressive effect of zoletyl-xylazine anesthesia on the heart and its chronotropic function, at a high frequency of atrial electrical stimulation, the depolarization gradient from the endocardium to the epicardium and from the apex to the base of the ventricles was preserved, there were only minor changes in the duration of the process of transmural depolarization of the walls of the ventricles of the heart. This indicates the resistance of activation of the ventricles of the heart of Wistar rats to the toxic effect of zoletyl-xylazine anesthesia.

作者简介

V. Nuzhny

Institute of Physiology of the Komi Scientific Center of the Ural Branch of the Russian Academy of Sciences,
Federal Research Center of the Komi Scientific Center of the Ural Branch of the Russian Academy of Sciences

Email: natanadya@mail.ru
Russia, Syktyvkar

N. Kibler

Institute of Physiology of the Komi Scientific Center of the Ural Branch of the Russian Academy of Sciences,
Federal Research Center of the Komi Scientific Center of the Ural Branch of the Russian Academy of Sciences

编辑信件的主要联系方式.
Email: natanadya@mail.ru
Russia, Syktyvkar

A. Tsvetkova

Institute of Physiology of the Komi Scientific Center of the Ural Branch of the Russian Academy of Sciences,
Federal Research Center of the Komi Scientific Center of the Ural Branch of the Russian Academy of Sciences

Email: natanadya@mail.ru
Russia, Syktyvkar

S. Kharin

Institute of Physiology of the Komi Scientific Center of the Ural Branch of the Russian Academy of Sciences,
Federal Research Center of the Komi Scientific Center of the Ural Branch of the Russian Academy of Sciences

Email: natanadya@mail.ru
Russia, Syktyvkar

A. Barkhaev

Institute of Physiology of the Komi Scientific Center of the Ural Branch of the Russian Academy of Sciences,
Federal Research Center of the Komi Scientific Center of the Ural Branch of the Russian Academy of Sciences

Email: natanadya@mail.ru
Russia, Syktyvkar

D. Shmakov

Institute of Physiology of the Komi Scientific Center of the Ural Branch of the Russian Academy of Sciences,
Federal Research Center of the Komi Scientific Center of the Ural Branch of the Russian Academy of Sciences

Email: natanadya@mail.ru
Russia, Syktyvkar

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