Effect of biliary tract external drainage on cytokine expression and histomorphology of intestine, liver, and lung in rats with hemorrhagic shock.
OBJECTIVE
To investigate the protective effect of biliary tract external drainage on cytokine expression and pathomorphism of intestine, liver, and lung in rats with hemorrhagic shock.


METHODS
Randomized, control animal study.


METHODS
This study was conducted at The Institution Digestive Surgery Research Laboratory of Shanghai Jiao Tong University.


METHODS
Sprague-Dawley rats.


METHODS
Biliary tract external drainage was performed by inserting a cannula into the bile duct. Hemorrhagic shock was induced by drawing blood from the carotid artery.


RESULTS
Twenty-four Sprague-Dawley rats were randomized to three equal groups of eight: sham shock; hemorrhagic shock; and hemorrhagic shock plus bile duct drainage. The messenger RNA expression of tumor necrosis factor-alpha, interleukin-6 in the intestine, liver, and lung tissue from the three groups were analyzed by reverse transcription-polymerase chain reaction. Tumor necrosis factor-alpha was analyzed in the bile of the rats by enzyme-linked immunosorbent assay. Histology of intestine, liver, and lung was performed in all groups by hematoxylin and eosin staining. The messenger RNA expression of tumor necrosis factor-alpha was significantly increased in the hemorrhagic shock group compared with the sham shock group (intestine 0.54 +/- 0.07 vs. 0.37 +/- 0.05, liver 1.01 +/- 0.06 vs. 0.56 +/- 0.07, lung 0.94 +/- 0.07 vs. 0.62 +/- 0.06). The messenger RNA expression of interleukin-6 was also significantly increased in the hemorrhagic shock group compared with the sham shock group (intestine 0.89 +/- 0.12 vs. 0.50 +/- 0.09, liver 1.07 +/- 0.10 vs. 0.57 +/- 0.12, lung 1.09 +/- 0.09 vs. 0.67 +/- 0.06). Biliary tract external drainage reduced significantly the messenger RNA expression of tumor necrosis factor-alpha (intestine 0.43 +/- 0.06 vs. 0.54 +/- 0.07, liver 0.74 +/- 0.18 vs. 1.01 +/- 0.06, lung 0.87 +/- 0.15 vs. 0.94 +/- 0.07) and interleukin-6 (intestine 0.60 +/- 0.11 vs. 0.89 +/- 0.12, liver 0.71 +/- 0.16 vs. 1.07 +/- 0.10, lung 0.88 +/- 0.25 vs. 1.09 +/- 0.09). The concentration of tumor necrosis factor-alpha in bile was significantly higher in the hemorrhagic shock group compared with the sham shock group (31.22 +/- 6.44 ng/mL vs. 15.49 +/- 3.64 ng/mL, p < .01). The histologic observation of the intestine, liver, and lung showed that the biliary tract external drainage significantly attenuate the putrescence and exfoliation of intestinal villi, denaturation and putrescence of hepatocytes, edema, and inflammatory cells infiltration of lung.


CONCLUSIONS
Biliary tract external drainage decreases the messenger RNA expression of tumor necrosis factor-alpha, interleukin-6 and attenuate the tissue injury of the intestine, liver, and lung in rats model of hemorrhagic shock. The gut-liver axis was implicated to play a crucial role in hemorrhagic shock-induced multiple organ dysfunction syndrome.
Liu
Yong-Jun
YJ
Surgical Intensive Care Unit, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China. liuyjun3@mail.sysu.edu.cn
Mao
En-Qiang
EQ
Ouyang
Bin
B
Chen
Juan
J
Tang
Yao-Qing
YQ
Huang
Shun-Wei
SW
Guan
Xiang-Dong
XD
D000818:Animals; D001646:Bile / Q000502:physiology*; D004322:Drainage; D004764:Enterohepatic Circulation / Q000235:genetics / Q000502:physiology; D015870:Gene Expression; D015850:Interleukin-6 / Q000097:blood* / Q000235:genetics; D007413:Intestinal Mucosa / Q000473:pathology*; D007511:Ischemia / Q000235:genetics / Q000503:physiopathology; D008099:Liver / Q000473:pathology*; D008168:Lung / Q000473:pathology*; D008297:Male; D009102:Multiple Organ Failure / Q000235:genetics / Q000473:pathology; D009336:Necrosis; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D012771:Shock, Hemorrhagic / Q000235:genetics* / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood* / Q000235:genetics
D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha