Bulletin of Medical and Biological Research

Summary. Structural and functional reconstruction of arterial bed of heart chambers may be due to various changes in hemodynamics in the great and small circles and the portal hepatic vein system, which is most often caused by portal hypertension, which can occur at removing large volumes of liver. Angioarchitectonics of the intraorganic channel of heart muscle in portal hypertension has not been fully studied. The aim of the study – morphometrically study  the features of remodeling of the arteries of ventricles  of heart in conditions of postresection portal  hypertension. Materials and Methods. Ventricular arteries of the heart of 94 white rats, divided into 3 groups were morphologically examined. Group 1 consisted of 15 animals, group 2 –  63 rats with simulated postresection portal hypertension, group 3 – 16 animals with a combination of postresection portal hypertension and multiorgan failure. Euthanasia of rats was performed by bloodletting under thiopental anesthesia. Histological micronutrients were made of the ventricles of heart, which determined the outer and inner diameters of the arteries of left and right ventricles of small caliber, the thickness of media and adventitial membrane, Wagenworth and Kernogan indices, endothelial cell height, diameter of their nuclei, nuclear-cytoplasmic relation, relative volume of damaged endothelial cells. Quantitative indicators were processed statistically. Results. Postresection portal hypertension leads to structural reconstruction of small ventricular arteries, which is characterized by thickening of the wall of studied vessels, narrowing of their lumen, marked changes in Wagenworth and Kernogan indices, deterioration of blood supply, nuclear-cytoplasmic relation disorders in endotheliocytes. The relative volume of damaged endothelial cells in conditions of postresection portal hypertension in the left ventricle was (19.20±0.30) %, in the right – (15.30±0.27) %, in case of multiple organ failure, respectively – (34.5±0.4) % and (24.30±0.36) %. Conclusions. Postresection portal hypertension leads to severe remodeling of the small arteries of left and right ventricles, which is characterized by thickening of their wall, narrowing of lumen, changes in the Kernogan and Wagenworth indices, damage to endothelial cells, endothelial trophic dysfunction and dystrophy and necrobyosis cellulae, tissues, foci of cellular infiltration and sclerosis. The revealed structural changes dominated in the left ventricle and in the combination of postresection portal hypertension with multiorgan failure

ventricles, arteries, postresection portal hypertension, morphometry