摘要
目的探讨失血性休克对内毒素的增敏作用及其机制，为失血性休克的治疗提供理论依据。方法采用生化、逆转录ＰＣＲ（ＲＴ－ＰＣＲ）及细胞原位杂交技术，观察了失血性休克条件下低剂量内毒素的作用及其可能机制，以及大鼠肝、肺、肾组织内脂多糖结合蛋白（ＬＢＰ）ｍＲＮＡ的表达。结果输入脂多糖（ＬＰＳ）后，失血性休克（ＨＳ）＋ＬＰＳ组家兔血压持续显著下降，血浆乳酸、β葡萄糖醛酸酶水平显著升高，与单纯ＬＰＳ或ＨＳ组比差异有显著意义。休克后２４小时，ＨＳ＋ＬＰＳ组动物全部死亡，而其余两组动物存活；ＲＴ－ＰＣＲ结果显示，休克及复苏后，大鼠肝、肺、肾组织内ＬＢＰｍＲＮＡ表达相继增多；细胞原位杂交结果表明，休克及复苏后，小鼠腹腔巨噬细胞内ＣＤ１４ｍＲＮＡ表达也明显增加。结论失血性休克能增敏内毒素的作用，其机制可能与休克上调ＬＢＰ／ＣＤ１４的表达有关。
Objective To study the increasing sensitivity to endotoxin induced by hemorrhagic shock and its mechanism. Methods Routine biochemical assay, reverse transcription polymerase chain reaction (RT PCR) and cell in situ hybridization were used to investigate the effects of low level endotoxin under hemorrhagic shock and its possible mechanism. Results In rabbits, blood pressure levels were significantly decreased, and plasma lactate and β glucuronidase (β G) levels increased in hemorrhagic shock (HS)+LPS group, all of which were significantly different from those in the LPS or HS group. All of the animals in the HS+LPS group were dead while those in the LPS or HS group survived 24 hours after shock. The results of RT PCR showed that expression of lipopolysaccharide binding protein (LBP) mRNA in the liver, lungs and kidneys was increased in rats after shock and resuscitation. The expression of CD14 mRNA in the peritoneal macrophages in mice was also enhanced after hemorrhagic shock and subsequent resuscitation showed by cell in situ hybridization. Conclusion Hemorrhagic shock can significantly increase the sensitivity to endotoxin possibly because of up regulation of LBP/CD14 after shock.
出处
《中华医学杂志》
CAS
CSCD
北大核心
1997年第4期282-285,共4页
National Medical Journal of China
