摘要
实验表明，单纯大剂量四氮化碳可严重损伤肝实质细胞，由于对枯否细胞的功能无明显影响，故未形成严重的内毒素血症。在四氯化碳损伤肝脏的同时，用二氧化硅抑制枯否细胞的功能则形成严重的内毒素血症，动物发生急性肝功能衰竭（肝昏迷与功能性肾衰竭）。从而进步证实了我们提出的肝功能衰竭发病机制——肠源性内毒素血症这一假说。
The resuIts indicated that
CCl4 of a large dose alone could induce severe injury of hepatic
cells, however,it could not affect the function of Kupffer cells and
no endotoxemia occured in rats. Silica could inhibit the func-tion of
Kupffer cells and induce severe endotoxemia. The rats gaven CCl4 +
SiO2 developed acute hepatic failure (hepatic coma and functional
renal failure).It was further proved that the hypothesis of
gut-origin endotox-emia may be the mechanism of hepatic failure.
