title: Colon ascendens stent peritonitis--a model of sepsis adopted to the rat: physiological, microcirculatory and laboratory changes.
abstract: The colon ascendens stent peritonitis (CASP) procedure creates an intestinal leakage of feces, resulting in diffuse peritonitis and polymicrobial sepsis. Mouse models of CASP have been used to study sepsis experimentally. The aim of the present study was to establish CASP sepsis in rats and to provide basic functional characteristics of this model. In analogy to the mouse model, 3 degrees of severity of CASP sepsis, 2 sublethal and 1 lethal, were established depending on the stent diameter. Radio-telemetric recordings in a sublethal model showed that the nonsurvivors remained hemodynamically stable until approximately 1 h before death, when heart rate and blood pressure fell rapidly. Intestinal microcirculatory changes were analyzed 3, 6, 12, and 18 h after CASP surgery using intravital microscopy in a sublethal model. After 18 h, the numbers of the leukocytes firmly adhering to the endothelium and of the ones temporarily interacting were significantly increased. The levels of IL-6 and IL-1beta increased continuously during the CASP experiments while remaining unchanged in the sham group. TNF-alpha and IL-10 levels of CASP animals reached a maximum after 12 h. In conclusion, a rat model of CASP sepsis has been established and characterized with regard to alterations in cardiovascular and microcirculatory function as well as plasma cytokine levels. In experimental settings where genetically engineered animals are not required, it will facilitate detailed examination of dynamic changes in integrated organ function during the course of sepsis and the investigation of treatment strategies.
authors.affiliation: Klinik für Chirurgie, Ernst-Moritz-Arndt-Universität, Greifswald, Germany. lustig@uni-greifswald.de
authors.forename: Martina Katja
authors.initials: MK
authors.lastname: Lustig
authors.forename: Vo Hoai
authors.initials: VH
authors.lastname: Bac
authors.forename: Dragan
authors.initials: D
authors.lastname: Pavlovic
authors.forename: Stefan
authors.initials: S
authors.lastname: Maier
authors.forename: Matthias
authors.initials: M
authors.lastname: Gründling
authors.forename: Olaf
authors.initials: O
authors.lastname: Grisk
authors.forename: Michael
authors.initials: M
authors.lastname: Wendt
authors.forename: Claus-Dieter
authors.initials: CD
authors.lastname: Heidecke
authors.forename: Christian
authors.initials: C
authors.lastname: Lehmann
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002448:Cell Adhesion; D003106:Colon / Q000098:blood supply / Q000382:microbiology / Q000473:pathology; D004195:Disease Models, Animal; D005243:Feces / Q000382:microbiology; D005260:Female; D006339:Heart Rate; D016753:Interleukin-10 / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007962:Leukocytes / Q000473:pathology; D008833:Microcirculation / Q000473:pathology / Q000503:physiopathology; D010538:Peritonitis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D011917:Rats, Inbred Lew; D018805:Sepsis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D015607:Stents; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10