Differential gene expression after hemorrhagic shock in rat lung.
BACKGROUND
We investigated the differential gene expression in rat lung after hemorrhagic shock (HS).


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Shih
Hsin-Chin
HC
Division of Surgery, Emergency Department, Taipei Veterans General Hospital, Taiwan, ROC. hcshih@vghtpe.gov.tw
Wei
Yau-Huei
YH
Lee
Chen-Hsen
CH
D000818:Animals; D020869:Gene Expression Profiling; D008168:Lung / Q000378:metabolism*; D008297:Male; D020411:Oligonucleotide Array Sequence Analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012771:Shock, Hemorrhagic / Q000378:metabolism*