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大白鼠肝在CCl_4中毒所引起肝硬化过程中,肝小叶结构被破坏。肝细胞中毒,坏死,脂肪游离增多。血窦因血流受阻而涨大。大部分肝细胞退变或坏死;部分残存而代偿性增生。结缔组织在坏变部分增生并包围肝小结而形成肝硬化。在肝硬化过程中,退变的肝细胞内脂滴增多。线粒体减少,成粒状或溶成一团。核糖核酸,糖元含量也随病变进展而减少。碱性磷酸酶反应增强。代偿性增生的肝细胞体积增大;肝细胞内线粒体增多,核糖核酸,糖元含量逐渐增多。在病变过程中出现冼多小型细胞。小型细胞出现在坏变的肝细胞区域,脂肪空泡附近及结缔组织内并随纤维的增加而减少。小型细胞含线粒体,核糖核酸,PAS反应及碱性磷酸酶反应均为阳性。文中讨论了肝细胞内细胞学和组织化学变化的意义;小型细胞的来源,与纤维形成的关系及纤维增生机制等问题。
Rat liver CCl_4 poisoning caused by cirrhosis of the liver lobular structure is destroyed. Hepatotoxicity, necrosis, increased free fat. Sinus blood flow due to blocked up. Most of the liver cell degeneration or necrosis; part of the residual compensatory proliferation. Connective tissue in the bad part of the proliferation and surrounding the formation of liver cirrhosis. During cirrhosis, there is an increase in lipid droplets in degenerated hepatocytes. Mitochondria reduce, into pellets or dissolved. Ribonucleic acid, glycogen content also decreases with lesion progression. Alkaline phosphatase reaction is enhanced. Compensatory hyperplasia of hepatocytes increased in size; hepatocytes increased mitochondria, ribonucleic acid, glycogen content gradually increased. Appeared in the lesion Sin small cells. Small cells appear in the area of degenerated hepatocytes, fat vacuoles, and connective tissue and decrease with increasing fibrosis. Small cells containing mitochondria, RNA, PAS and alkaline phosphatase reaction were positive. The significance of cytological and histochemical changes in hepatocytes, the origin of small cells, the relationship with the formation of fibroids and the mechanism of fibrogenesis were discussed.