失血性休克对内毒素血症小鼠CD14 mRNA表达的影响

Effect of hemorrhagic shock on endotoxemia and expression of CD14 mRNA

观察家兔失血性休克合并门静脉源性轻度内毒素血症动物血压、血浆乳酸、β—G水平和死亡率的变化,结合小鼠腹腔巨噬细胞内CD14mRNA的表达,并对休克增敏内毒素作用的机制进行初步分析。结果表明,输入LPS后,失血休克(HS)+LPS组动物血压持续显著下降,血浆乳酸、β—G水平显著升高,且分别明显低于或高于单纯LPS或HS组。休克后24h,HS+LPS组动物全部死亡,而其余两组动物存活;细胞原位杂交结果显示,休克及复苏后,腹腔巨噬细胞胞浆内CD14mRNA表达增多。提示失血性休克能显著增敏内毒素作用,其机制可能与休克上调CD14表达有关。

This experiment was to investigate the changes of blood pressure, plasma lactate and β-glucuronidase(β-G)levels, and mortality rate after hemorrhagic shock and subsequent low-level portal endotoxemia in rabbits. With combination of expression of CD14 mRNA in the peritoneal macrophages in mice after hemorrhagic shock, intented to study the mechanism of increaing sensitivity to endotoxin by shock. It was found that blood pressure levels were significantly decreased, and plasma lactate and β-G levels increased in hemorrhagic shock(HS)+LPS group. They were significantly different at each time point after infusion of LPS compared with LPS or HS group. All the animals in HS+LPS group were dead while those in LPS or HS group survived 24 hours following shock. Results from cell in situ hybridization showed that expression of CD14 mRNA in the peritoneal macrophages was enhanced after hemorrhagic shock and subsequent resuscitation. It is sug gested that the significantly increased sensitivity to endotoxin after hemorrhagic shock might be due to up-regulation of CD14 after shock.