中文摘要：

瞄准：建立暴发性的肝的失败(FHF ) 的一个适当首领模型。方法：第一次，我们由 amatoxin 和内毒素的 intraperitoneal 注入在 Macaca mulatta 建立了 FHF 的一个大动物模型。临床的特征，生物化学的索引，组织病理学说和肖像画法被检验动态地调查动物模型的进步和结果。结果：我们的结果证明酶和浆液 bilirubin 显著地被增加， enzyme-bilirubin 分离出现了在毒素管理以后的 36 h。凝结活动显著地被减少。逐渐地败坏的 parenchymal 反常被磁性的回声成像(MRI ) 和 ultrasonography 在 48 h 检测。肝活体检视分别地在 36 h 和 49 h 显示出显著 hepatocyte 脂肪变性和巨大的 parenchymal 坏死。尸体显示出肝的典型黄萎缩。模型的肝的 encephalopathy 被肝的昏迷， MRI 和服的浮肿的病理学的变化也证实。extrahepatic 机关机能障碍的致命的效果被他们的生物化学的索引，成像和组织病理学说排除。结论：我们建立了 FHF 的一个适当大首领模型，它密切类似于诊所案例，并且能被用于 FHF 并且为潜在的医药治疗的评估的机制的调查。

英文摘要：

AIM： To establish an appropriate primate model of ful- minant hepatic failure （FHF）. METHODS： We have, for the first time, established a large animal model of FHF in Macaca mulatta by intra-peritoneal infusion of amatoxin and endotoxin. Clinical features, biochemical indexes, histopathology and ico- nography were examined to dynamically investigate the progress and outcome of the animal model. RESULTS： Our results showed that the enzymes and serum bilirubin were markedly increased and the enzyme-bilirubin segregation emerged 36 h after toxin administration. Coagulation activity was significantly decreased. Gradually deteriorated parenchymal abnor- mality was detected by magnetic resonance imaging （MRI） and ultrasonography at 48 h. The liver biopsy showed marked hepatocyte steatosis and massive pa- renchymal necrosis at 36 h and 49 h, respectively. The autopsy showed typical yellow atrophy of the liver. He- patic encephalopathy of the models was also confirmed by hepatic coma, MRI and pathological changes of cerebral edema. The lethal effects of the extrahepatic organ dysfunction were ruled out by their biochemical indices, imaging and histopathology. CONCLUSION： We have established an appropriate large primate model of FHF, which is closely similar to clinic cases, and can be used for investigation of the mechanism of FHF and for evaluation of potential medi- cal therapies.