论文部分内容阅读
笔者观察了大鼠失血性休克（ＨＳ）对内毒素诱导肿瘤坏死因子α（ＴＮＦα）产生的影响及其细胞来源，并结合休克后组织内脂多糖结合蛋白（ＬＢＰ）ｍＲＮＡ的表达变化，对其分子机制进行了初步分析。研究结果显示，静脉注射ＬＰＳ后９０ｍｉｎ，ＨＳ＋ＬＰＳ组血浆ＴＮＦα水平分别较ＨＳ组高２０倍（Ｐ＜０．０１），ＬＰＳ组高２．７倍（Ｐ＜０．０５）；休克和复苏后，外周血白细胞产生ＴＮＦα的能力明显受抑，而肝Ｋｕｐｆｅｒ＇ｓ细胞产生ＴＮＦα的能力却明显增强；休克后不仅肝组织内ＬＢＰｍＲＮＡ表达增多，肺、肾组织内ＬＢＰｍＲＮＡ也相继表达增加。研究结果提示，失血性休克能显著增敏内毒素诱导ＴＮＦα的产生作用，其机制可能与休克后组织内ＬＢＰ表达上调有关，组织巨噬细胞群（如Ｋｕｐｆｅｒ细胞）可能是休克后细胞因子产生的主要来源。
The author observed the effects of hemorrhagic shock (HS) on TNF-α induced by endotoxin and the origin of the cells, combined with the changes of lipopolysaccharide binding protein (LBP) mRNA expression in the tissues after shock, Molecular mechanism for a preliminary analysis. The results showed that at 90min after intravenous injection of LPS, the level of TNFα in HS + LPS group was 20 times higher than that in HS group (P <0.01), and 2.7 times higher in LPS group (P <0.05). After shock and resuscitation, The ability of peripheral blood leukocytes to produce TNFα was significantly inhibited, while the ability of liver Kupfer’s cells to produce TNFα was significantly enhanced. Not only the expression of LBP mRNA increased in liver tissue, but also the expression of LBP mRNA in lung and kidney tissues. The results suggest that hemorrhagic shock can significantly enhance endotoxin-induced TNFα production, and its mechanism may be related to the up-regulation of LBP expression in the post-shock tissue. Tissue macrophage population (such as Kupfer cells) may be cytokines after shock The main source.