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观察了大鼠失血性休克（ＨＳ）条件下小剂量内毒素（ＬＰＳ，１ｕｇ／ｋｇ）对肿瘤坏死因子α（ＴＮＦａ）的诱生作用及其细胞来源。结果显示，静脉注射ＬＰＳ后９０ｍｉｎ，ＨＳ＋ＬＰＳ组血浆ＴＮＦａ水平分别较ＨＳ组高２０倍（Ｐ＜０．０１），较ＬＰＳ组高２．７倍（Ｐ＜０．０５）。体外研究结果显示，复苏后即刻，外周血白细胞（ＰＷＢＣ）体外产生ＴＮＦａ的能力明显受抑，分别较休克前和假手术组低５５．８％和３６．５％（Ｐ＜０．０１，Ｐ＜０．０５），至复苏后３ｈ，仍显著受抑。肝Ｋｕｐｆｆｅｒ细胞体外产生ＴＮＦａ的能力在休克和复苏后明显增强，较假手术组高１１０％（Ｐ＜０．０１）。研究结果提示，失血性休克能显著增敏内毒素诱导ＴＮＦａ的产生作用，这可能与休克增敏组织巨噬细胞有关。
The effects of low dose lipopolysaccharide (LPS, 1 ug / kg) on tumor necrosis factor alpha (TNFa) induced by hemorrhagic shock (HS) and the origin of the cells were observed. The results showed that plasma TNFa level in HS + LPS group was 20 times higher than that in HS group 90min after intravenous injection of LPS (P <0.01), 2.7 times higher than LPS group (P <0.05). In vitro studies showed that the ability of peripheral blood leukocytes (PWBC) to produce TNFa in vitro was significantly inhibited immediately after resuscitation, which were 55.8% and 36.5% lower than those before shock and sham operation respectively (P <0.01, P <0.05), 3h after resuscitation, still significantly inhibited. The ability of hepatic Kupffer cells to produce TNFa in vitro was significantly enhanced after shock and resuscitation, which was 110% higher than that of the sham-operated group (P <0.01). The results suggest that hemorrhagic shock can significantly sensitize endotoxin-induced TNFa production, which may be related to shock-sensitized tissue macrophages.