Evensen S A, Pickering R J, Batbouta J, Shepro D
Eur J Clin Invest. 1975 Nov 21;5(6):463-9. doi: 10.1111/j.1365-2362.1975.tb00478.x.
The role of complement activation in the pathogenesis of endothelial injury caused by bacterial endotoxin was investigated in the rat. DNA synthesis in aortic endothelium was compared 48 hours after an intravenous injection of endotoxin (50 - 500 mug) in normal rats and in rats depleted of haemolytic complement by purified cobra venom factor. At the time of endotoxin administration the rats treated with cobra venom factor had less than 3% of the normal haemolytic complement level, their fibrinogen level was increased and clot retraction was impaired. Endotoxin stimulated endothelial DNA synthesis to the same degree in normal and in complement-depleted rats. Cobra venom factor alone did not stimulate endothelial DNA synthesis. The complement-depleted rats given 500 mug endotoxin were less thrombocytopenic than normal rats at the time of sacrifice, but the difference was not statistically significant. We conclude that the injurious effect endotoxin has on endothelium is not mediated by activation of late components of complement.
在大鼠中研究了补体激活在细菌内毒素所致内皮损伤发病机制中的作用。比较了正常大鼠和经纯化眼镜蛇毒因子耗尽溶血补体的大鼠静脉注射内毒素（50 - 500微克）48小时后主动脉内皮中的DNA合成情况。在内毒素给药时，用眼镜蛇毒因子处理的大鼠溶血补体水平低于正常水平的3%，其纤维蛋白原水平升高且血块回缩受损。内毒素在正常大鼠和补体耗尽的大鼠中刺激内皮DNA合成的程度相同。单独的眼镜蛇毒因子不刺激内皮DNA合成。处死时，给予500微克内毒素的补体耗尽大鼠的血小板减少程度低于正常大鼠，但差异无统计学意义。我们得出结论，内毒素对内皮的损伤作用不是由补体晚期成分的激活介导的。
