title: Comparing hemodynamics, blood gas analyses and proinflammatory cytokines in endotoxemic and severely septic rats.
abstract: Lipopolysaccharide (LPS) is often used in short-term models of inflammation. Since endotoxemia and sepsis are different entities we have recently established a short-term sepsis model in rats induced by cecal ligation and incision (CLI). This retrospective study was conducted in order to identify similarities and differences between both experimental approaches. 32 anesthetized/ventilated male rats from the following four groups were analysed (each n=8): CTRL-group (0.9% NaCl i.v.); LPS-group (5mg/kg i.v.); SHAM-group (laparotomy); CLI-group (1.5 cm blade incision). Mean arterial blood pressure (MAP) and blood gas parameters (arterial base excess (BE) and pH) were continuously recorded. Total observation time was 300 min. Plasma samples were obtained afterwards. LPS and CLI induced significant arterial hypotension and metabolic acidosis compared to CTRL- or SHAM-group, respectively. Yet, between the LPS- and CLI-groups, there were no differences in MAP, BE and pH. LPS significantly induced IL-1β, IL-6 and TNF-α in the plasma. In contrast, CLI showed a clear tendency towards increased IL-1β and IL-6 plasma levels and did not affect TNF-α. Our results indicate that the CLI sepsis model is suitable for short-term investigations on hemodynamic alterations and blood gas analyses during sepsis. 300 min after the proinflammatory insult, plasma concentrations of IL-1β and IL-6 in the plasma remain considerably lower after CLI compared to endotoxemia. Low TNF-α concentrations 300 min after sepsis induction could be interpreted as considerable immunosuppression during CLI sepsis.
authors.affiliation: Pharmazentrum Frankfurt/ZAFES, Hospital of the Johann Wolfgang Goethe-University Frankfurt/Main, Theodor-Stern-Kai 7, Frankfurt/Main, Germany.
authors.forename: Patrick
authors.initials: P
authors.lastname: Scheiermann
authors.forename: Sandra
authors.initials: S
authors.lastname: Hoegl
authors.forename: Christian
authors.initials: C
authors.lastname: Hofstetter
authors.forename: Josef
authors.initials: J
authors.lastname: Pfeilschifter
authors.forename: Bernhard
authors.initials: B
authors.lastname: Zwissler
authors.forename: Heiko
authors.initials: H
authors.lastname: Mühl
authors.forename: Kim A
authors.initials: KA
authors.lastname: Boost
authors.forename: Bertram
authors.initials: B
authors.lastname: Scheller
mesh_terms: D000138:Acidosis; D000818:Animals; D001784:Blood Gas Analysis; D002432:Cecum / Q000276:immunology / Q000378:metabolism* / Q000601:surgery; D002478:Cells, Cultured; D016207:Cytokines / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D019446:Endotoxemia / Q000097:blood* / Q000139:chemically induced / Q000276:immunology*; D006439:Hemodynamics; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008297:Male; D023421:Models, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D008070:Lipopolysaccharides