Effect of Natural Cytokine Complex on the Structure and Metabolism of the Cardiac Conduction System in the Myocardium under Normally and Increased Hemodynamic Load


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Effect of natural complex of cytokines with activity of IL-1, IL-2, IL-6, TNF, MIF, and GTFβ on the structure and metabolism of conduction cardiomyocytes was assessed in the control and under acute experimental aortic stenosis. After systemic administration of the cytokine complex in the control, structural abnormalities were revealed in a relatively low number of conduction cardiomyocytes; their relative number increased in the left ventricle and interventricular septum. When the complex was administered against the background of aortic stenosis, morphological changes in the conduction system were seen in a significant number of cells with their plasma imbibition, especially in the left ventricle and interventricular septum. Systemic administration of the natural cytokine complex inhibited the major metabolic processes in the conduction system, both in the control and under conditions of sharply increased hemodynamic load. In conduction cardiomyocytes, deceleration of glycolysis and citric acid cycle, inhibition of oxidation of free fatty acids and their metabolites, and suppression of shuttle mechanisms and biosynthetic reactions were observed. Increased blood levels of cytokines, primarily of the proinflammatory ones, can cause structural and metabolic disturbances in the cardiac conduction system and promote the development of arrhythmias, especially in case of sharply increased hemodynamic load.

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M. Tverskaya

N. I. Pirogov Russian National Research Medical University

编辑信件的主要联系方式.
Email: mstverskaya@mail.ru
俄罗斯联邦, Moscow

L. Gankovskaya

N. I. Pirogov Russian National Research Medical University

Email: mstverskaya@mail.ru
俄罗斯联邦, Moscow

V. Sukhoparova

N. I. Pirogov Russian National Research Medical University

Email: mstverskaya@mail.ru
俄罗斯联邦, Moscow

A. Virganskii

N. I. Pirogov Russian National Research Medical University

Email: mstverskaya@mail.ru
俄罗斯联邦, Moscow


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