Purpose of the study. Studying the features of microcirculation, functional state and anatomy of the heart using the “Holiday Heart” syndrome model in rats we developed.Materials and methods. Experiments were carried out on white outbred male rats. The “Holiday Heart” syndrome was modeled as follows: animals received a 10 % aqueous ethanol solution as the only source of fluid for the first 10 days, then tap water for 10 days, and again a 10 % aqueous ethanol solution for the next 10 days. One day after the end of the repeated intake of alcohol, the animals were taken into the experiment. Animals that received free access to tap water served as control. Some rats in the experimental group (n = 10) had an echocardiogram recorded before the start of the experiment, and on the 31st day of the experiment, after which the level of microcirculation of blood and lymph in the brain and heart was measured using laser Doppler flowmetry. In the remaining animals (n = 10), microcirculation of blood and lymph in the brain and heart was assessed on the 3rd day of alcohol deprivation.Results. Analysis of the obtained data showed that in the conditions of the “Holiday Heart” syndrome model, significant changes occur in the anatomy, functional activity and geometry of the heart: there is a significant thinning of the anterior wall of the left ventricle heart (LV), an increase in systolic and diastolic volumes and sizes of the LV and a significant (p = 0.0018) decrease in its inotropic function. These changes occur against the background of a significant (p = 0.0081) decrease in the level of blood microcirculation in the myocardium, however, on the 3rd day of deprivation, blood flow in the microvessels of the heart increases statistically significantly (p = 0.0285).Conclusion. In model experiments reproducing the “Holiday Heart” syndrome, it was shown for the first time that ethanol causes significant changes in the microcirculation, anatomy, functional activity and geometry of the left ventricle of the heart, which, apparently, can play a key role in the formation of myocardial electrical instability pathognomonic for this syndrome.

Introduction. It is known that the allosteric effector of cAMP, in addition to protein kinase A, is the Epac regulatory proteins, which in cardiomyocytes play a key role in the electromechanical coupling control and their rhythmic activity. However, under pathological conditions, abnormal activity of Epac proteins is responsible for the hypertrophy and fibrosis of cardiomyocytes and the initiation of cardiac arrhythmias. Objective. To study the cardiotropic activity of the compound N,2,4,6-tetramethyl-N-(pyridin-4-yl)benzolsulfonamide (code ZMEI-3), which potentially has the properties of Epac protein antagonists, in models of cardiac arrhythmias and alcoholic cardiomyopathy ( ACMP).Materials and methods. Experiments were carried out on outbred male rats. The antiarrhythmic activity of the ZMEI-3 compound was assessed in models of aconitine and reperfusion arrhythmias, and the cardioprotective activity in a translational model of ACM, which is formed after 24 weeks of forced intake of 10 % ethanol.Results. Using a model of reperfusion arrhythmias in rats, it was shown that the ZMEI-3 compound (2 mg/kg/day for 7 days i.p.) reduces the incidence of life-threatening arrhythmias, including ventricular fibrillation. In conditions of formed ACMP, the studied compound (2 mg/kg/day for 28 days i.p.) increased the inotropic function of the heart, which was judged by the value of the left ventricular ejection fraction. Histological analysis showed that in conditions of formed ACMP, the ZMEI-3 compound reduces the severity of morphological signs of alcoholic heart damage.Conclusions. Compound ZMEI-3, when used in a course, has a pronounced antiarrhythmic effect and reduces the severity of alcohol-related heart failure.

Purpose of the study. Comparative evaluation of echocardiographic and morphometric dimensions of the rat heart left ventricle. Materials and methods. The study included 10 outbred male rats weighing 160–180 g. The size of the heart left ventricle was assessed using echocardiography and morphometry. The measurements were carried out according to standard protocols. To perform morphometric measurements, hearts were stopped in systole with a lethal dose (1.0 mg/kg) of 0.025 % strophanthin K solution, and in diastole, by immersing the hearts in a chilled physiological solution (calcium-free medium). Results. It was shown that the systolic size of the left ventricle of the heart according to echocardiography is 1.79Ѓ}0.10 mm, and morphometry 1.64Ѓ}0.09 mm (p = 0,302); diastolic size of the left ventricle, respectively, 3.42Ѓ}0.16 mm and 3.66Ѓ}0.17 mm (р = 0,318). The detected discrepancies do not exceed 10 % and, apparently, are due to the fact that the physiological dimensions of the heart left ventricle are measured by a non-invasive echocardiographic method, and for morphometric measurements of the dimensions in the systole, the heart was stopped by injection of strophanthin K, which entails an overload of heart cells with Ca2+ ions and as a result, contracture of cardiomyocytes; post-mortem cardiac arrest in diastole, in a calcium-free environment, is accompanied by a loss of cardiac muscle tone and, therefore, dilatation of the left ventricle will naturally be greater than physiological. Conclusion. Noninvasive echocardiographic measurement of the size of the heart left ventricle fully reflects the actual size of the left ventricle of the rat heart (the difference does not exceed 10 %), i. e. echocardiographic measurements are valid.