Bacterial translocation and tumor necrosis factor-alpha gene expression in experimental hemorrhagic shock.
OBJECTIVE
To investigate whether bacterial translocation is the causative mechanism underlying cytokine production during hemorrhagic shock.


METHODS
Prospective, randomized, unblinded animal study.


METHODS
Surgical research laboratories of Shiga University of Medical Science.


METHODS
Male Sprague-Dawley rats.


METHODS
The rats were randomly divided into three groups. Each animal was anesthetized with pentobarbital, given a continuous infusion of 0.9% saline, and monitored for blood pressure. The normoxic and sham shock groups breathed room air, whereas the hyperoxic shock group was administered 100% oxygen. Except in the sham shock group, blood was withdrawn to induce a hemorrhagic shock state, then the shed blood was reinfused. Sixty minutes after the induction of hemorrhagic shock, arterial blood cultures were performed in all three groups. The animals were then killed, and their mesenteric lymph nodes (MLNs) were harvested for bacterial culture. The terminal ileum, liver, spleen, kidney, lung, and MLNs were also collected for histologic study by in situ hybridization.


RESULTS
In the bacteriologic study, the prevalence of bacterial translocation was 0% (0/11) in the hyperoxic shock group, 55% (6/11) in the normoxic shock group, and 0% (0/9) in the sham shock group. In the in situ hybridization study, tumor necrosis factor-alpha gene expression was detected only in the ileal tissue, MLNs, and spleens of the normoxic shock group. Blood cultures were sterile in all three groups.


CONCLUSIONS
Bacterial translocation occurred in MLNs within 1 hr of hemorrhage. Hemorrhagic shock causes tumor necrosis factor-alpha gene expression as well as bacterial translocation in MLNs, but not in the liver, in this model. Bacterial translocation was prevented by hyperoxia early in the course of hemorrhagic shock. Hyperoxia also prevented tumor necrosis factor-alpha gene expression along the bacterial invasion route.
Tani
T
T
First Department of Surgery, Shiga University of Medical Science, Otsu-shi Shiga, Japan. MXG01037@nifty.ne.jp
Fujino
M
M
Hanasawa
K
K
Shimizu
T
T
Endo
Y
Y
Kodama
M
M
D000818:Animals; D018988:Bacterial Translocation / Q000235:genetics* / Q000502:physiology; D005786:Gene Expression Regulation / Q000502:physiology; D007082:Ileum / Q000473:pathology; D008198:Lymph Nodes / Q000473:pathology; D008297:Male; D010100:Oxygen / Q000097:blood; D019879:Paneth Cells / Q000473:pathology; D015347:RNA Probes; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D012771:Shock, Hemorrhagic / Q000235:genetics* / Q000473:pathology; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology; D013154:Spleen / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*
D015347:RNA Probes; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D010100:Oxygen