慢性盐酸肝炎时胃黏膜和小肠氮能系统的状态

M. Kulmanova, R. Sabirova
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引用次数: 1

摘要

慢性heliotrinine诱导肝炎(CHH),在脑室和肠粘膜组织中形成内皮功能障碍,其特征是一氧化氮水平降低。在CHH中,eNOS活性降低是由于内毒素对胃粘膜组织和肠道的作用,从肝脏进入中央血流。同时,它们启动iNOS并形成ОNO 2 -,从而抑制eNOS。这似乎是CHH中肝脏内毒素作用的增强作用,以响应脑室和肠粘膜eNOS活性的抑制,iNOS的启动,ОNO 2 -形成-一种重要的细胞毒性/细胞抑制剂,增强增殖和凋亡过程,因此,脑室和肠粘膜肠上皮的高水平降解和脱屑。研究了CHH时小肠粘膜和肠道内氮能系统的指标呈一个方向变化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
STATE OF GASTRIC MUCOSA AND SMALL INTESTINE NITRO-ERGIC SYSTEM DURING CHRONIC HELIOTRINE-INDUCED HEPATITIS
In chronic heliotrineinduced hepatitis (CHH), in t he tissues of the mucous membrane of the ventricle and bowels an endothelial dysfunction, characterized by a decreased level of NO is formed. In CHH, eNOS activity decreases due to the action of endotoxins on the gastric mucosa tissue and bowels entering to the central bloodstream from the liver. At the same time, they initiate iNOS and formation of ОNO 2 � that leads to inhibition of eNOS. It appears as potentiating effect of endotoxins' action produced in the liver in CHH in response to the inhibition of mucous membrane of the ventricle and bowels eNOS activity, initiation of iNOS, ОNO 2 � formation - an important cytotoxic / cytostatic compound, enhancing the proliferative and apoptotic processes, as a result, a high level of degradation and desquamation of the intestinal epithelium of the mucous membrane of the ventricle and bowels. Studied indicators of nitroergic system in the mucosa of the ve ntricle and bowels at CHH change in one direction.
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