Assessment of features of morphometric structural changes in the testes at conditions of postresection portal hypertension
Keywordstestes, portal hypertension, multiple organ failure, morphometry
Introduction. Postresection portal hypertension leads to complex general biological processes that occur and develop in the organs and systems of the body during its adaptation to a new level of life . It should be noted that detailed and objective knowledge of compensatory-adaptive processes in the testes during resection of various volumes of the liver, their role in the development of organ failure to date have been insufficiently studied and need to be addressed.
Objective of the research: to study morphometric structural changes of testes in the conditions of postresection portal hypertension and multiorgan failure.
Materials of the research and their discussion. The testes of 40 white male rats were divided into 3 groups studied morphologically. Group 1 consisted of 12 intact animals, 2 - 18 rats with postresection portal hypertension, 3 - 10 animals with postresection portal hypertension and poliorganic failure. Euthanasia of rats was performed by bloodletting under thiopental anesthesia a month after the start of the experiment. Micropreparations from the testes stained hematoxylin-eosin, toluidine blue, using the Weigert method, van Gieson, Mallory, Morphometrically, on the testicular micropreparations, the diameters of the testicles tubules, the thickness of their walls, the number of cells of the epithelio-spermatogenic layer in the tubule, the number of Sertoli cells per tubule, the tubulo-interstitial index, the stromal-parenchymal ratio, the Leydigas index, the sperm index, were determined. Quantitative morphological parameters were processed statistically.
Results of the research and their discussion. It was found that the investigated morphometric indices of the testes in the 2 and 3 groups of observations varied markedly in comparison with the control values. Thus, the diameter of the seminile tubules in the conditions of postresection portal hypertension was statistically significantly (p˂0.001) decreased by 11.8 %, with the development of multiple organ failure - by 34.0 % (p<0.001), and the number of cells of the epithelio-spermatogenic layer in tubules respectively by 11.3 % and 32.9 % (p˂0.001), which indicated the presence of atrophy of the studied structures.
The wall thickness of the tubules in the 2 group increased by 8.8 %, in the 3 group - by 26.9 % (р<0.001), and the Leydig index - by 22.9 % and 57.8 %, respectively (р<0.001). The number of Sertoli cells in one testicle tubule in the 2nd group decreased by 1.6 % and in the 3rd by 8.06 % (p <0.001).
Stromal-parenchymal ratios in the testes with simulated pathology statistically significantly increased (р<0.001) by 11.3 % (р˂0.01) and 31.8 % (р˂0.001), while the tubulo-interstitial index decreased respectively by 8.9 % (p<0.001) and 31.8 % (p<0.001). The revealed changes of the investigated morphometric parameters showed a pronounced increase in the number of stroma in the testes. The spermatogenesis intensity index also decreased by 2.9 % (p<0.05) and 38.8 % (p<0.001), respectively.
Obtained morphometric parameters indicate that the simulated pathology leads to a decrease in the diameter of the tubules and the thickening of their walls. In the latter, optically sclerosis was observed. In the lumen of the seminiferous tubules, histologic examination revealed spermatocytes of the first order and spermatogonia, rarely observed spermatocytes of the second order. Protein detritus and rarely sperm were detected in the tubules.
Conclusions. So postresection portal hypertension and multiorgan failure lead to pronounced structural restructuring of the vascular, interstitial and endocrine components of the testes, characterized by dilatation, plethora, varicose extensions, stasis, hemorrhage, perivasal swelling of the vessels gemomicrocirculatory bad and, hyperplasia, moderate hypertrophy Leydig cell dystrophy. The detected morphological changes dominate in multiple organ failure.
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