摘要
实验采取先激活或抑制枯否细胞功能，后用硫代乙酰胺引发大鼠的严重肝损伤，以观察不同功能状态枯否细胞在急性肝功能衰竭发生发展中的作用。实验结果表明，激活枯否细胞功能，可使肝损伤与肠源性内毒素血症减轻；抑制枯否细胞功能，肝损伤虽无明显改变，但肠源性内毒素血症加重，同时出现严重肾功能障碍与肝性昏迷。上述结果提示。
In an attempt to elucidate the role of
functional status of kupffer cells in the acute hepatic failuer,We
established the model of severe hepatic injury in rat by TAA
injuction and inhibiting the function ofkupffer cells.The results
indicated that in the activated group hepatic injury and gut-
derivedendotoxemia induced by TAA were reduced, whereas in the
suppressed group this hepatic inuury did notchange,gut-derived
endotoxemia was aggravated )accompanying with disorder of renal
function andhepatic coma。The above results suggested that gut-
derived endotoxemia played a decisive role in acutehepatic failure。
