МОРФОМЕТРИЧНІ АСПЕКТИ АНАЛІЗУ СТРУКТУРНОЇ ПЕРЕБУДОВИ ВЕНОЗНОГО РУСЛА КАМЕР СЕРЦЯ В УМОВАХ ПОСТРЕЗЕКЦІЙНИХ ЛЕГЕНЕВОЇ ТА ПОРТАЛЬНОЇ ГІПЕРТЕНЗІЙ

A significant socio-medical direction is the study of the structure of the human heart and experimental animals in connection with the wide spread and growth of cardiovascular diseases. Functional and structural changes in the venous bed, which carries out drainage and actively responds to increased pressure in the pulmonary and portal systems, have not been sufficiently studied in the heart. Aim. To conduct a comparative morphometric analysis of the features of the structural rearrangement of the venous bed of the heart chambers in the conditions of post-resection pulmonary and portal hypertension. Material and methods. The hearts of 46 white male rats, which were divided into three groups, were morphologically examined. The first group included 16 intact animals, the 2nd – 15 rats with post-resection portal hypertension, the 3rd – 15 experimental animals with post-resection pulmonary hypertension. In the left and right ventricles of the heart, the diameter of postcapillary venules and venules, the outer and inner diameters of venous vessels, the thickness of their walls, the height of endotheliocytes, the diameter of their nuclei, the nuclear-cytoplasmic ratio in endotheliocytes, and the relative volume of damaged cells were measured. The results. In the course of the study, changes in the quantitative morphological indicators of the vessels of the venous bed of the heart were observed compared to the control ones. The diameter of post-capillary venules and venules of the left ventricle increased by 5.0 % and venules by 4.9 % (p<0.05) in post-resection portal hypertension (p<0.05), and by 16, respectively, in post-resection arterial pulmonary hypertension. 8 % (p<0.001) and 17.4 % (p<0.001). The outer diameter of the venous vessels of the right ventricle increased statistically significantly (p<0.05) by 3.5 % in post-resection portal hypertension, and by 21.6 % in pulmonary hypertension (p<0.001). The internal diameter of the venous vessels of the right ventricle increased by 6.4 % (p<0.05) in post-resection portal hypertension, and by 39.4 % (p<0.001) in post-resection pulmonary hypertension. In the second observation group (post-resection portal hypertension), media thickness (p<0.01) decreased by 3.4 %, and in the 3rd group (post-resection pulmonary hypertension) – by 25.4 % (p<0.01). The height of the endotheliocytes of venous vessels and the diameter of their nuclei, the nuclear-cytoplasmic index of the right ventricle in post-resection portal hypertension were slightly changed, which indicated the stability of structural cellular homeostasis. The relative volume of damaged endotheliocytes in the studied vessels in post-resection portal hypertension increased 2.3 times (p<0.001), and in post-resection pulmonary hypertension it increased 20.05 times (p<0.001), which can lead to endothelial dysfunction of the venous bed hearts In the 3rd experimental group, the height of the endotheliocytes of the studied vessels of the right ventricle with post-resection pulmonary hypertension decreased by 10.6 % (р<0.05), the diameter of the nuclei decreased by 6.1 %, and the nuclear-cytoplasmic ratio in the endotheliocytes exceeded the similar control indicator by 9.0 % (р<0.01), which indicated a violation of structural cellular homeostasis. Conclusion. Post-resection portal and pulmonary hypertensions lead to a pronounced structural rearrangement of the venous vascular bed and heart components. The detected pathomorphological changes were dominant in the right ventricle in post-resection arterial pulmonary hypertension and the left ventricle in post-resection portal hypertension.