Mochida S, Ogata I, Hirata K, Ohta Y, Yamada S, Fujiwara K
First Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Gastroenterology. 1990 Sep;99(3):771-7. doi: 10.1016/0016-5085(90)90967-6.
When rats received endotoxin 48 hours after two-thirds liver resection, 50% of them died within 12 hours with massive hepatic necrosis at a dose that did not affect sham-operated rats. In the hepatic sinusoids, fibrin deposition and endothelial cell destruction occurred 5 hours after endotoxin administration. When antithrombin III concentrate was infused concomitantly with endotoxin administration, all rats survived 12 hours, and the extent of hepatic necrosis and the deranged serum glutamic pyruvic transaminase values were significantly attenuated at 5 hours compared with those in the control rats. Similar improvements in the incidence of mortality and liver injury were observed after treatment with gum arabic before hepatectomy. The stimulatory state of Kupffer cells based on the ability to produce superoxide anions estimated by formazan deposition after liver perfusion with nitro blue tetrazolium and phorbol myristate acetate was increased between 24 and 72 hours after operation. This increase disappeared after gum arabic treatment. It is concluded that massive hepatic necrosis can occur as a result of sinusoidal fibrin deposition provoked by endotoxin in partially hepatectomized rats. Activated Kupffer cells may contribute to this provocation.
当大鼠在三分之二肝切除术后48小时接受内毒素时，其中50%在12小时内死亡，出现大面积肝坏死，而该剂量对内毒素未处理的假手术大鼠没有影响。在内毒素给药5小时后，肝血窦内出现纤维蛋白沉积和内皮细胞破坏。当在内毒素给药的同时输注抗凝血酶III浓缩物时，所有大鼠存活12小时，与对照大鼠相比，5小时时肝坏死程度和血清谷丙转氨酶值的紊乱情况明显减轻。肝切除术前用阿拉伯胶治疗后，死亡率和肝损伤发生率也有类似改善。根据用硝基蓝四氮唑和佛波酯肉豆蔻酸酯灌注肝脏后通过甲臜沉积估计的产生超氧阴离子的能力，库普弗细胞的刺激状态在术后24至72小时增加。阿拉伯胶治疗后这种增加消失。结论是，部分肝切除大鼠中，内毒素引发的血窦纤维蛋白沉积可导致大面积肝坏死。活化的库普弗细胞可能促成了这种激发。
