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Bacterial translocation and tumor necrosis factor-α gene expression in experimental hemorrhagic shock
- 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 Except in the sham shock group, blood was withdrawn to induce a hemorrhagic shock state, then the shed blood was reinfused.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.
- Subjects :
- Male
Paneth Cells
Pathology
medicine.medical_specialty
Spleen
Shock, Hemorrhagic
Critical Care and Intensive Care Medicine
Rats, Sprague-Dawley
Ileum
medicine
Animals
Mesenteric lymph nodes
RNA, Messenger
Hyperoxia
Kidney
Tumor Necrosis Factor-alpha
business.industry
RNA Probes
Pathophysiology
Rats
Oxygen
medicine.anatomical_structure
Gene Expression Regulation
Bacterial Translocation
Shock (circulatory)
Arterial blood
Tumor necrosis factor alpha
Lymph Nodes
medicine.symptom
business
Signal Transduction
Subjects
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