THE ENDOGENOUS INTOXICATION IN THE ORGANISM OF EXPERIMENTAL ANIMALS AT JEJUNUM DAMAGE IN CONDITIONS OF POSTRESECTION PORTAL HYPERTENSION
DOI:
https://doi.org/10.11603/mcch.2410-681X.2018.v0.i3.9551Keywords:
endogenous intoxication, jejunum, postresection portal hypertensionAbstract
Introduction. Removal of large volumes of liver parenchyma is complicatedby postresection portal hypertension. The latter leads to a morphological rearrangement of the organs of the portal hepatic vein, the damage to their structures, and the growth of endogenous intoxication, which is not sufficiently investigated in the case at jejunum damage at these pathological conditions.
The aim of the study– to learn the characteristics of endogenous intoxication of the experimental animals in the case of damage of the jejunumin conditions of postresection portal hypertension.
Research Methods. The studies were performed on 60 white male rats, which were divided into 4 groups. The first group consisted of 15 intact animals, 2–15 rats, in which we removed 31.5% of liver parenchyma, 3–15 animals after resection 42% of liver parenchyma, 4–15 rats in which we removed 58,1% liver parenchyma. One month after beginning of the experiment euthanasia of experimental animals was performed by bloodletting under conditions of thiopental anesthesia. The state of endogenous intoxication by the concentration of TBC-active products, oxidative modification of proteins, and the content of molecules of the average mass were determined. Histologic section from the jejunum stained with hematoxylin-eosin, for van Giason, Mallory, Weigert, and toluidine blue. Histostereometrically, the relative volumes of damaged epithelial cells, muscle cells, and endothelial cells were determined. Quantitative values were processed statistically.
Results and Discussion. In rats, one month after resection, 42% and 58.1% of the liver parenchyma, enlargement of the hepatic portal vein, enlargement of the mesenteric veins and the visible venous bed of the small and large intestines were observed. The evidence of the presence of portal hypertension is detected. Mucous membrane of the jejunum is full-blooded, edematous, with single cells of point hemorrhages. In the wall of the jejunum we revealed dystrophy, necrobiosis of epithelial cells, myocytes, endothelial cells, stromal structures, infiltrative and sclerotic processes, which were more pronounced during resection of 58.1% of liver parenchyma. Relative volumes of damaged investigated structures increased significantly month after resection of 42% of liver parenchyma and the largest values they reached when removed 58.1% of the volume of this organ, indicating a significant defeat of the jejunum under simulated experimental conditions. In the case of the detected lesions of the jejunum, endogenous intoxication of the body was expressed, which was confirmed by a significant (p<0.05) increase in the content of molecules of the average mass in serum, TBK-active products, oxidative modificationof proteins. The degree of endogenous intoxication of the body at postresection portal hypertension depended on the severity of the damage of the jejunum.
Conclusions. Resection of large volumes of liver parenchyma leads to the development of postresection portal hypertension, damage structures of the jejunum and endogenous intoxication of the body, which is accompanied by an increase in the content molecules of the average mass, the oxidative modification of proteins, the activation of peroxidation oflipids. The degree of endogenous intoxication of the body depends on the removed volume of liver parenchyma and the severity of damage the structures of the jejunum.
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