[Increased sensitivity to endotoxin and its molecular mechanism after hemorrhagic shock].

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 beta-glucuronidase (beta-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 CD144 mRNA in the peritoneal macrophages in mice was also enhanced after hemorrhagic shock and subsequent resuscitation showed by cell in situ hybridization.

CONCLUSIONS

Hemorrhagic shock can significantly increase the sensitivity to endotoxin possibly because of up-regulation of LBP/CD14 after shock.