title: Gut ischemia and mesenteric synthesis of inflammatory cytokines after hemorrhagic or endotoxic shock.
abstract: The intestine plays a major role in the pathophysiology of multiorgan failure. Although the systemic inflammatory response might be induced by endotoxin released through bacterial translocation, other factors such as intestinal ischemia might be implicated. We investigated the relationship between intestinal ischemia-reperfusion and cytokine release in rat models of hemorrhagic or endotoxic shock. Plasma levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), lactate, and endotoxin, as well as macrophage TNF-alpha and IL-6 mRNA expression, were assessed at the end of shock and resuscitation. Hemodynamic changes and lactate levels suggested the presence of intestinal ischemia in both models. Mesenteric levels of TNF-alpha and IL-6 were increased by hemorrhage and further increased after saline resuscitation. Similar results were obtained with mRNA cytokine gene expression in macrophages. Endotoxin was not detectable in the hemorrhagic group. Endotoxic shock also increased production of cytokines, which, in contrast to hemorrhage, was not further increased by resuscitation. These results suggest that intestinal ischemia-reperfusion upon hemorrhage and resuscitation may be a major trigger for cytokine gene expression in the absence of endotoxin.
authors.affiliation: Institut Fédératif de Recherche Multidisciplinaire sur les Peptides, Institut National de la Santé et de la Recherche Médicale Unité 78, Bois-Guillaume, France.
authors.forename: F
authors.initials: F
authors.lastname: Tamion
authors.forename: V
authors.initials: V
authors.lastname: Richard
authors.forename: S
authors.initials: S
authors.lastname: Lyoumi
authors.forename: M
authors.initials: M
authors.lastname: Daveau
authors.forename: G
authors.initials: G
authors.lastname: Bonmarchand
authors.forename: J
authors.initials: J
authors.lastname: Leroy
authors.forename: C
authors.initials: C
authors.lastname: Thuillez
authors.forename: J P
authors.initials: JP
authors.lastname: Lebreton
mesh_terms: D000818:Animals; D016207:Cytokines / Q000096:biosynthesis*; D004731:Endotoxins / Q000097:blood; D006439:Hemodynamics; D006470:Hemorrhage / Q000150:complications / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism*; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D007422:Intestines / Q000098:blood supply*; D007511:Ischemia / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D019344:Lactic Acid / Q000097:blood / Q000378:metabolism; D017737:Macrophages, Peritoneal / Q000378:metabolism; D008297:Male; D008643:Mesentery / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012772:Shock, Septic / Q000150:complications / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D016207:Cytokines; D004731:Endotoxins; D018836:Inflammation Mediators; D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D019344:Lactic Acid