枯否细胞在急性实验性肝功能衰竭发生中的作用  

The Role of Kupffer Cells in Acute Hepatic Failure

作　　者：马京香[1] 高国洁 

机构地区：[1]山东省血液中心,济南250014 [2]山东省煤矿总医院

出　　处：《医学检验与临床》2003年第1期13-15,共3页Medical Laboratory Science and Clinics

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)。从而进一步证实了我们提出的肝功能衰竭发病机制一肠源性内毒素血症这一假说。The results indicated that CCI4, 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 function of Kupffer cells and induce severe endotoxemia. The rats gaven CCI4 + SiO2 developed acute hepatic failure (hepatic coma and functional renal failure). It was further proved that the hypothesisof gut-origin endotox-emia may be the mechanism of hepatic failure.

关 键 词：肝功能衰竭 内毒素血症 二氧化硅 

分 类 号：R575.3[医药卫生—消化系统]