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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。
The changes of blood pressure, plasma lactate, β-G level and mortality in rabbits with hemorrhagic shock associated with portal venous mild endotoxemia were observed. The expression of CD14 mRNA in mouse peritoneal macrophages was observed and sensitized by shock The toxin mechanism of the initial analysis. The results showed that the blood pressure of LPS + LPS group continued to decrease significantly and Lactate and β-G levels were significantly increased after LPS administration, which were significantly lower than or higher than those of LPS or HS group alone. All animals in HS + LPS group died at 24 h after shock, while the other two groups survived. The results of in situ hybridization showed that the expression of CD14 mRNA in peritoneal macrophages increased after shock and resuscitation. It is suggested that hemorrhagic shock can significantly sensitize endotoxin, which may be related to the up-regulation of CD14 expression by shock.