Hnatyuk M. S., Chernetsky A. A., Tatarchuk L. V., Stets N. Ja.

MORPHOLOGICAL CHANGES IN THE THYROID ARTERIAL BED AT LONG-TERM POSTRESECTION PORTAL HYPERTENSION AND MULTIORGAN FAILURE

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About the author:

Hnatyuk M. S., Chernetsky A. A., Tatarchuk L. V., Stets N. Ja.

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MORPHOLOGY

Type of article:

Scientific article

Annotation:

It is well known that hypertension in the portal vein system often leads to pronounced changes in systemic hemodynamics and is complicated by variceal dilatation and bleeding from gastroesophageal and rectal veins, hepatorenal and hepatopulmonary syndromes, enteropathy, encephalopathy, and multiple organ failure. Resection of large liver volumes is also complicated by post-resection portal hypertension. The structures and vascular bed of the thyroid gland, an important organ of the endocrine system, are altered not only under the influence of adverse endogenous and exogenous factors but also in various hemodynamic disorders. The morphology of the arterial vasculature of the thyroid gland under conditions of portal hypertension has not been fully elucidated. Therefore, a comprehensive study of the thyroid arteries in portal vein hypertension is warranted. Morphologically and morphometrically, the thyroid arteries were studied in 15 intact male Wistar rats, 30 animals with postoperative portal hypertension, and 17 animals with a combination of postoperative portal hypertension and multiple organ failure. On histological sections of the thyroid gland, the area of the arteries, their lumen, intima, adventitia, Wogenworth and Kernogan indices, endothelial cell area, nuclear area, nuclear-to-cytoplasmic ratios, and the volume of damaged endothelial cells were determined. Quantitative data were processed statistically. It was established that post-resection portal hypertension leads to pronounced structural remodeling of the thyroid arteries, characterized by an increase in the area of the studied vessels, media, and adventitia, as well as the Wogenworth index, while the lumen, intima, and endothelial cell areas decrease, the Kernogan index declines, and the arterial permeability is reduced. Endothelial cells are damaged, accompanied by endothelial dysfunction, impaired organ perfusion, hypoxia, dystrophy, apoptosis, necrosis of endothelial cells, thymocytes, and stromal structures, foci of cellular infiltrates, and sclerosis. The observed morphological changes in the thyroid arteries are most pronounced in the development of multiple organ failure.

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Publication of the article:

«Bulletin of problems biology and medicine», 2025 Issue 4, 179, 305-312 pages, index UDC 616.36-089.87-06.616-91]-092.9

DOI:

10.29254/2077-4214-2025-4-179-305-312