Gut J P, Schmitt S, Bingen A, Anton M, Kirn A
J Infect Dis. 1982 Nov;146(5):594-605. doi: 10.1093/infdis/146.5.594.
Four to six days after colectomy, rats resisted a challenge of frog virus 3 that in sham-operated animals led to lethal hepatitis. Furthermore, the beneficial effect of colectomy was lost after intravenous administration of a dose of bacterial endotoxin as small as 0.01 100% lethal dose. The protection was related to neither a different distribution of the virus in body organs nor a stimulation of the reticuloendothelial system. The virus-induced early events--destruction of liver sinusoidal cells with leakage of cathepsin D into serum and inhibition of liver macromolecular synthesis--evolved similarly in both groups of rats. After an identical consumption of complement at the beginning of infection, a renewal in complement activity in the protected rats contrasted with an increasing deficiency in the control animals. The protective role of colectomy seems to be related to the suppression of the main source of bacterial endotoxin.
结肠切除术后四至六天，大鼠能抵抗蛙病毒3的攻击，而在假手术动物中，该病毒会导致致命性肝炎。此外，静脉注射低至0.01个100%致死剂量的细菌内毒素后，结肠切除术的有益效果消失。这种保护作用既与病毒在身体器官中的不同分布无关，也与网状内皮系统的刺激无关。两组大鼠中，病毒诱导的早期事件——肝窦细胞破坏，组织蛋白酶D泄漏至血清以及肝脏大分子合成受到抑制——的发展情况相似。在感染初期消耗相同量的补体后，受保护大鼠的补体活性得以恢复，而对照动物的补体缺乏却日益严重。结肠切除术的保护作用似乎与抑制细菌内毒素的主要来源有关。
