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Bacterial translocation and tumor necrosis factor-α gene expression in experimental hemorrhagic shock

Authors :
Mitsuhiro Fujino
Masashi Kodama
Yoshihiro Endo
Tomoharu Shimizu
Kazuyoshi Hanasawa
Tohru Tani
Source :
Critical Care Medicine. 28:3705-3709
Publication Year :
2000
Publisher :
Ovid Technologies (Wolters Kluwer Health), 2000.

Abstract

OBJECTIVE To investigate whether bacterial translocation is the causative mechanism underlying cytokine production during hemorrhagic shock. DESIGN Prospective, randomized, unblinded animal study. SETTING Surgical research laboratories of Shiga University of Medical Science. SUBJECTS Male Sprague-Dawley rats. INTERVENTIONS 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 Except in the sham shock group, blood was withdrawn to induce a hemorrhagic shock state, then the shed blood was reinfused.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. MEASUREMENTS AND MAIN 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.

Details

ISSN :
00903493
Volume :
28
Database :
OpenAIRE
Journal :
Critical Care Medicine
Accession number :
edsair.doi.dedup.....2b450e352d58b5682d555d5667a108ef
Full Text :
https://doi.org/10.1097/00003246-200011000-00028