目的探讨大鼠慢性肝病基础上诱导的急性肝衰竭(慢加急性肝衰竭)模型肝脏组织病理学动态特征。方法购入雄性SD大鼠,以50%四氯化碳植物油溶液腹腔注射,每3天1次,连续3个月(第一个月1.5 mL/kg体质量,第2、3个月2.0 mL/kg体质量),建立大鼠肝硬化模型,对照组腹腔注射植物油溶液。肝硬化模型成立后,腹腔注射2 g/kg体质量D-氨基半乳糖(D-Galac-tosamine,D-Gal),建立肝硬化基础急性肝衰竭模型,并动态进行病理染色及电镜观察。结果大鼠慢加急性肝衰竭模型制备良好,所有大鼠出现明显的腹水及黄疸症状,出现假小叶结构及细胞凋亡等。D-Gal急性攻击后,短时间内出现组织水肿、脂肪变性明显,大片嗜酸性变性。电镜上开始胞浆疏松、亚细胞器变形、糖原减少等,逐渐出现细胞器变少、异性结构、核固缩等现象。最终整个细胞器形态结构破坏,碎屑样小体出现及细胞溶解坏死。结论肝硬化基础上药物急性攻击时除了细胞凋亡外,中毒所引起的溶解坏死后期参与大量肝细胞死亡。 Objective To investigate the histopathological characteristics of liver in acute liver failure (acute and acute liver failure) induced model of chronic liver disease in rats. Methods Male Sprague-Dawley rats were purchased and injected intraperitoneally with 50% CTC vegetable oil solution every 3 days for 3 months (1.5 mL / kg body weight for the first month, 2.0 mL for the 2nd and 3rd month / kg body weight), the establishment of rat model of liver cirrhosis, the control group intraperitoneal injection of vegetable oil solution. After establishment of the cirrhosis model, 2-g / kg D-Galactosamine (D-Gal) was intraperitoneally injected to establish the model of acute liver failure in cirrhotic liver. The liver cirrhosis models were observed by dynamic pathological staining and electron microscopy. Results The models of acute and chronic hepatic failure in rats were well prepared. All the rats showed obvious signs of ascites and jaundice, pseudolobule structure and apoptosis. After D-Gal acute attack, tissue edema occurred in a short period of time, with obvious fatty degeneration and large-area eosinophilic degeneration. Electron microscope began loose cytoplasm, subcellular organelle deformation, glycogen reduction, and gradually appear less organelles, heterosexual structure, nuclear pyknosis and so on. Eventually the entire organelle morphology and structure destruction, debris-like bodies appear and cell lysis necrosis. Conclusions In addition to apoptosis, acute hepatotoxicity induced by hepatotoxicity is involved in a large number of hepatocyte death during the later phase of lytic necrosis.