We investigated the differential gene expression in rat lung after hemorrhagic shock (HS).
A controlled HS model in rats was used. Male Sprague-Dawley rats were randomly segregated into 2 groups, sham and HS. Samples of lung were procured from rats 2 hours after HS and resuscitation. Commercially available gene chips for rat cDNA microarray and software packages were used for the gene expression profile study.
Compared with sham-shock rats, 98 genes were upregulated in HS rat lung. Most upregulated genes were responsible for inflammation (pro-inflammatory or anti-inflammatory cytokines, cognate receptors, and signal transduction for inflammation), protein activation (kinase and phosphatase), oxidation (oxidative and antioxidative enzymes), and apoptosis (apoptosis and anti-apoptosis). Eleven genes were downregulated after HS.
HS may induce upregulation of positive and negative control genes responsible for inflammation, oxidation, protein metabolism and apoptosis, that is, a vulnerable period may develop in the host after HS. Overwhelming inflammatory response or immunosuppression may occur once a second hit, such as infection, ensues. Understanding, on a genome scale, how an organism responds to HS may facilitate the development of enhanced treatment modalities for HS.