title: Evidence favoring the role of the gut as a cytokine-generating organ in rats subjected to hemorrhagic shock.
abstract: There is increasing evidence of an association between intestinal injury and the development of a septic state and distant organ failure. Since this phenomenon can occur in the absence of detectable systemic bacterial translocation (BT), we tested the hypothesis that shock-induced intestinal injury will result in the gut becoming a cytokine-generating organ by measuring interleukin 6 (IL-6) and tumor necrosis factor (TNF) levels in the portal blood, cardiac blood, and intestinal lymph of rats subjected to sham, 30, 60, or 90 min of hemorrhagic shock (30 mm Hg). These blood and lymph samples, as well as the mesenteric lymph nodes (MLN), spleens, and livers, were cultured for translocating bacteria. Although all the portal and cardiac blood samples were sterile, the portal blood levels of TNF and IL-6 were increased to a greater extent than simultaneously obtained cardiac blood samples in rats subjected to 60 or 90 min of shock (p < .05). The lymph IL-6 levels increased but were similar between the groups. BT was limited to the MLN and occurred in a dose-dependent fashion with 38, 63, and 100% of the animals having culture-positive MLNs after 30, 60, or 90 min of shock, respectively. In conclusion, after hemorrhagic shock, the gut appears to become a cytokine liberating organ even in the absence of detectable bacteria in the portal circulation.
authors.affiliation: Medical Center, Louisiana State University, Shreveport 71130, USA.
authors.forename: E A
authors.initials: EA
authors.lastname: Deitch
authors.forename: D
authors.initials: D
authors.lastname: Xu
authors.forename: L
authors.initials: L
authors.lastname: Franko
authors.forename: A
authors.initials: A
authors.lastname: Ayala
authors.forename: I H
authors.initials: IH
authors.lastname: Chaudry
mesh_terms: D000818:Animals; D016470:Bacteremia / Q000097:blood / Q000209:etiology; D001419:Bacteria / Q000302:isolation & purification; D016207:Cytokines / Q000096:biosynthesis*; D005263:Femoral Artery; D006321:Heart; D015850:Interleukin-6 / Q000032:analysis; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000098:blood supply / Q000382:microbiology; D007511:Ischemia / Q000209:etiology / Q000378:metabolism / Q000382:microbiology*; D008099:Liver / Q000382:microbiology; D008196:Lymph / Q000737:chemistry; D008198:Lymph Nodes / Q000382:microbiology; D008297:Male; D008643:Mesentery / Q000382:microbiology; D011169:Portal Vein; D051381:Rats; D012771:Shock, Hemorrhagic / Q000150:complications / Q000378:metabolism*; D013047:Specific Pathogen-Free Organisms; D013154:Spleen / Q000382:microbiology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D016207:Cytokines; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha