QUANTITATIVE MORPHOLOGICAL FEATURES OF THE STRUCTURAL REARRANGEMENT OF THE VENOUS BLOOD VESSELS OF THE PROSTATE GLAND IN POST-RESECTION PORTAL HYPERTENSION

Abstract

Aim: Using quantitative morphological methods to study the peculiarities of the structural reconstruction of the venous bad of the prostate at the conditions of post-resection portal hypertension. Materials and Methods: Morphologically, the venous bed of the prostate of 15 intact white rats, 30 animals with post-resection portal hypertension, 17 rats with a combination of post-resection portal hypertension with hepatargia, enteral, cardiac, and renal insufficiency was studied. Rats were slaughtered one month after the start of the experiment by bloodletting under general thiopental anesthesia. Morphometry of the venous blood vessels of the prostate gland was performed on histological specimens, during which the diameter of the postcapillary venules, the diameter of the venules, the external diameter of the venous vessels, the internal diameter of the venous vessels, the thickness of the wall of the venous vessels was determined. Also it was studied the height of endothelial cells, diameter of their nuclei, nuclear-cytoplasmic ratio in these cells, relative volume of damaged endothelial cells, density of vessels of microcirculatory bed per 1 mm² of prostate tissue. Results: It was found that resection of the left and right lobes of the liver leads to the development of postresection portal hypertension and pronounced remodeling of the vessels of the venous bed of the prostate gland, which was characterized by the expansion of the capillary venules of the prostate by 36.5%, with the occurrence of multiple organ failure by 38.5% (р<0.001 ), an increase in the lumen of veins, thinning of their wall, atrophy, dystrophy, and necrobiosis of endothelial cells, disruption of structural cellular homeostasis, endothelial dysfunction, hypoxia, dystrophic-necrotic changes in cells, stromal structures, infiltration, and sclerosis. Morphological changes in the structures of the prostate dominated when post-resection portal hypertension was combined with multiple organ failure. Conclusions: Post-resection portal hypertension in laboratory sexually mature white male rats leads to pronounced remodeling of the venous bed of the prostate gland, which is characterized by the expansion of the lumen of the vessels, thinning of their walls, atrophic, dystrophic and necrobiotic changes in endothelial cells, a violation of structural cellular homeostasis in them, endothelial dysfunction, hypoxia, dystrophic-necrotic changes in cells, stromal structures, infiltration and sclerosis. Morphological changes in the structures of the prostate dominated when post-resection portal hypertension was combined with multiple organ failure.