抄録
Background. Alcoholic cardiomyopathy is considered to be the major somatic complication of alcoholism. This pathology occupies confidently the leading position in the structure of mortality from circulatory diseases. In patients with alcoholic cardiomyopathy the risk of malignant cardiac arrhythmias, including atrial fibrillation, is extremely high. So, the main aim of this work was to estimate features of depolarization of atria and study the dynamics of changes in the expression of regulatory proteins in biopsies of tissues taken from different parts of the atria in previously developed translational model of alcoholic cardiomyopathy in rats (Kryzhanovskii S.A. et al., 2017).
Methods. Adult male albino rats were given 10 % ethanol as the only source of fluid and ad libitum access to food. By the end of 24th week of forced alcohol exposure the sequence of depolarization of the atrial subepicardium has been studied by polyelectrocardiographic test with multichannel surface electrodes for simultaneous registration of 32 unipolar epicardial electrogram, and the gene expression of exchange protein directly activated by cAMP Epac1, Epac2, as well as calmodulin were measured using quantitative polymerase chain reaction.
Results. In the aged intact rats the wave of excitation is uniformly distributed from the region of the sinoatrial node to right and left atrium. In rats with alcoholic cardiomyopathy, however, the additional locus of early excitation in the region of gaps of the pulmonary veins in the left atrium is formed. In biopsy tissues from animals with alcoholic cardiomyopathy hyperexpression of signaling protein Epac2 was revealed. The level of mRNA Epac2 in the left atrium has increased in 3,2 times and in the right atrium in 3 times compared to intact rats. A reduction in expression Epac1 and calmodulin responsible for formation of dilated heart failure in alcoholic cardiomyopathy were also revealed.
Conclusions. In rats with alcoholic cardiomyopathy atypical excitation is formed in the region of the gaps of pulmonary veins, which can initiate the development of atrial fibrillation. Hyperexpression of signaling protein Epac2 was revealed from anomalous centers of excitement, corresponding with data about their role in trigger mechanisms of arrhythmia.
