Gdanska N. M., Hnatjuk M. S., Tatarchuk L. V., Monastyrska N. Ja.
The structural and functional reorganization of the myocardium can be caused by various changes in hemodynamics in the great and small circles of blood circulation and the system of the hepatic portal vein. In the latter, these changes are most often caused by portal hypertension, which often occurs when large volumes of liver are removed. It should be noted that remodeling of ventricular structures in postresection portal hypertension has been insufficiently studied. The purpose of research – to histostereometrically study the features of remodeling of the structures of the ventricles of the heart at postresection portal hypertension. Methods and Material. The features of remodeling the ventricular structures of the heart of 65 adult white male rats, which were divided into 3 groups, were histostoreometrically studied. The 1 group consisted of 20 intact animals, the 2 – 30 rats, which simulated postresection portal hypertension by removing the left and right lateral lobes of the liver, the 3 – 15 animals with postresection portal hypertension and multiorgan failure. Thirty days after the start of the experiment, euthanasia of experimental animals was performed by bloodletting under conditions of thiopental anesthesia. Histological micropreparations were prepared from the left and right ventricles of the heart, on which morphometry of ventricular structures was performed, in which the diameters of left and right ventricular cardiomyocytes, their nuclei, nuclear-cytoplasmic relations, relative volumes of cardiomyocytes, capillaries, stroma, stromal-cardiomyocyte, capillary-cardiomyocyte relations, relative volumes of damaged cardiomyocytes were determined. Quantitative indicators were processed statistically. Results and Discussion. A comprehensive analysis of the obtained indicators showed that the diameter of left ventricular cardiomyocytes in postresection portal hypertension increased by 24.8% (p <0.001) compared with a similar control histostereometric parameter, and in the event of multiple organ failure – by 32.0% (p<0.001), diameters of cardiomyocyte nuclei – by 17.2% (p<0.001) and 18.6% (p<0.001), respectively. Nuclear-cytoplasmic ratios in these cells in postresection portal hypertension decreased by 11.6% (p<0.01), in combination with postresection portal hypertension with multiorgan failure – by 18.8% (p<0.001), and capillary-cardiomyocyte ratios respectively by 22.9% (p<0.001) and 27.8% (p<0.001). The relative volume of damaged cardiomyocytes in the left ventricle at postresection portal hypertension increased 5.5 times, in the field of organ failure – 10.3 times, the relative volume of stromal structures also increased markedly. Capillary-cardiomyocyte ratios in the right ventricle in portal hypertension with a pronounced statistically significant difference (p<0.001) decreased by 12.5%, with the development of multiple organ failure – by 17.2%, the relative volume of damaged cardiomyocytes increased by 3.05 times and 7.1 times (p<0.001). Postresection portal hypertension leads to a pronounced remodeling of the ventricular structures of the heart, which was characterized by hypertrophy of cardiomyocytes, changes in their nuclear-cytoplasmic relations, an increase in the relative volumes of stroma, damaged heart muscle cells, pronounced disorders of stromal-cardiomyocyte, capillary-cardiomyocyte relations. The revealed morphological changes in a left ventricle at a combination of a postresection portal hypertension with multiorgan insufficiency dominated.
«Bulletin of problems biology and medicine» Issue 4 (162), 2021 year, 251-255 pages, index UDK 616.36-089.87-06:616-091]-092.9
