摘要
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 present study was to observe the effect of rat hemorrhagic shock on tumor necrosis factor α(TNFα) induced by small dose endotoxin(LPS) and its cellular sources.It was found that plasma TNFα levels in HS+LPS group were 20 fold higher than those in HS group ( P <0 01), and 2 7 fold higher than those in LPS group ( P <0 05) 90min after injection of LPS.It was show in vitro experiment that the capacity of peripheral white blood cells to produce TNFα in response to LPS stimulation was significantly decreased by 55 8%( P <0 01) and 36 5%( P <0 05),compared with the pre shock levels and sham group respectively at the end of resuscitation following shock,and stillmarkedly inhibited 3 hours after resuscitation,while the capacity of hepatic Kupffer cells to produce TNFα was significantly increased by 110%, compared with the sham group( P <0 01) after shock and resuscitation.It is suggested that induction of TNFα in response to LPS stimulation could be significantly increased after hemorrhagic shock,which may be mainly related to the primed tissue macrophages in shock.
出处
《解放军医学杂志》
CAS
CSCD
北大核心
1996年第6期412-413,共2页
Medical Journal of Chinese People's Liberation Army
