Konovalenko S. O.

PECULIARITIES OF THE STRUCTURAL TRANSFORMATION OF THE TESTICULAR VENOUS BED AT POSTRESECTION PORTAL HYPERTENSION


About the author:

Konovalenko S. O.

Heading:

MORPHOLOGY

Type of article:

Scentific article

Annotation:

Intraorganic venous bed plays an important role in the drainage of venous blood and its impairments and structural changes leads to marked circulatory disorders, which significantly affects the functioning of organs and systems. It should be noted that the testicular vein shave not been sufficiently investigated at postresection portal hypertension. Purpose – to study the structural changes of the venous structures of testicles at postresection portal hypertension. Methods of research. Using a complex of morphological methods, the testicular veins of 45 laboratory white adult male rats, divided into groups of 3, were investigated. The 1st group consisted of 15 intact animals; the 2nd included 15 rats after resection of the left lateral hepatic lobe (31.5% of the liver parenchyma), the 3rd included 15 animals after removal of the right and left lateral lobes of the liver (58.1%). Animal euthanasia was performed by bloodletting under thiopental sodium anesthesia 1 month after the start of the experiment. The testicular cuts were fixed in 10% neutral formalin solution and after conducting through ethyl alcohols of increasing concentration were placed in paraffin blocks according to the conventional method. Microtome sections 5-7 μm thick after deparaffinization were stained with hematoxylin-eosin, van Gieson, Mallory, Weigert, toluidine blue. At the morphometric examination of the testicular micropreparations, the diameter of the postcapillary venules, the diameter of the venules, the outer and inner diameters, the height of the endothelial cells of the venous vessels, the diameter of their nuclei, nuclear-cytoplasmic ratios in these cells, the relative volume of damaged cells were determined. Morphometric parameters were processed statistically. Result and discussion. The analysis of the obtained data revealed that the removal of 31.5% of the liver parenchyma did not lead to the marked hemodynamic disturbances in the portal hepatic vein. The structure of the venous bed did not change significantly. Resection of the left and right lateral lobes of the liver (58.1% of its parenchyma) led to the development of postresection portal hypertension, which was confirmed by the enlargement and plethora of the portal hepatic vein, mesenteric veins, as well as veins of the small and large intestine, splenomegaly. In this case, the structure of the venous bed of the testicles changed significantly. Thus, the diameter of the postcapillary venules of the testicle was increased by 24.2%, venules – by 21.7%, and veins – by 18.1% (p<0.001). The internal diameter of the venous vessels exceeded the control by 18.75% (p <0.001). The height of venous endothelial cells under these experimental conditions decreased by 5.0% (p<0.01), the diameter of their nuclei by 1.7% (p <0.05). Nuclear-cytoplasmic ratios increased by 9.3%with a high degree of confidence (p<0.001), indicating a violation of structural cellular homeostasis. The relative volume of damaged endothelial cells in the venous vessels of the testicle increased 16.8-fold (p<0.001). Expansion of the venous bed of the testicles in postresection portal hypertension is accompanied by venous plethora, which is complicated by hypoxia, which leads to dystrophy, necrobiosis of cells and tissues of the testicles, and in the long term to infiltrative and sclerotic processes. Conclusions. The obtained data indicate that structural changes in the venous bed of the testicles atpostresection portal hypertension significantly disrupt the drainage of venous blood from the specified organ, worsen its trophic supply and play an important role in the pathomorphogenesis of its lesion.

Tags:

testicle, venous bed, postresection portal hypertension

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Publication of the article:

«Bulletin of problems biology and medicine» Issue 3 (152), 2019 year, 297-300 pages, index UDK [611.631+612.616+616.681]:612.273.2

DOI: