title: A murine model for the study of edema induced intestinal contractile dysfunction.
abstract: BACKGROUND
  We have published extensively regarding the effects of edema on intestinal contractile function. However, we have found the need to expand our model to mice to take advantage of the much larger arsenal of research support, especially in terms of transgenic mouse availability and development. To that end, we have developed and validated a hydrostatic intestinal edema model in mice.
  
  
  METHODS
  Male C57 Black 6 mice were subjected to a combination of high volume crystalloid resuscitation and mesenteric venous hypertension in an effort to induce hydrostatic intestinal edema. Wet to dry ratios, myeloperoxidase activity, mucosal injury scoring, STAT-3 nuclear activation, phosphorylated STAT-3 levels, NF-κB nuclear activation, myosin light chain phosphorylation, intestinal contractile activity, and intestinal transit were measured to evaluate the effects of the model.
  
  
  RESULTS
  High volume crystalloid resuscitation and mesenteric venous hypertension resulted in the development of significant intestinal edema without an increase in myeloperoxidase activity or mucosal injury. Edema development was associated with increases in STAT-3 and NF-κB nuclear activation as well as phosphorylated STAT-3. There was a decrease in myosin light chain phosphorylation, basal and maximally stimulated intestinal contractile activity, and intestinal transit.
  
  
  CONCLUSIONS
  Hydrostatic edema in mice results in activation of a signal transduction profile that culminates in intestinal contractile dysfunction. This novel model allows for advanced studies into the pathogenesis of hydrostatic edema induced intestinal contractile dysfunction.
authors.affiliation: Department of Pediatric Surgery, University of Texas Medical School at Houston, Houston, TX 77030, USA.
authors.forename: S K
authors.initials: SK
authors.lastname: Shah
authors.forename: S D
authors.initials: SD
authors.lastname: Moore-Olufemi
authors.forename: K S
authors.initials: KS
authors.lastname: Uray
authors.forename: F
authors.initials: F
authors.lastname: Jimenez
authors.forename: P A
authors.initials: PA
authors.lastname: Walker
authors.forename: H
authors.initials: H
authors.lastname: Xue
authors.forename: R H
authors.initials: RH
authors.lastname: Stewart
authors.forename: G A
authors.initials: GA
authors.lastname: Laine
authors.forename: C S
authors.initials: CS
authors.lastname: Cox
mesh_terms: D000818:Animals; D002467:Cell Nucleus / Q000378:metabolism; D000077324:Crystalloid Solutions; D003593:Cytoplasm / Q000378:metabolism; D004487:Edema / Q000503:physiopathology*; D005769:Gastrointestinal Motility / Q000502:physiology*; D005772:Gastrointestinal Transit / Q000502:physiology; D006973:Hypertension / Q000503:physiopathology; D045823:Ileus / Q000503:physiopathology; D007422:Intestines / Q000503:physiopathology*; D007552:Isotonic Solutions / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009119:Muscle Contraction / Q000502:physiology; D009130:Muscle, Smooth / Q000503:physiopathology*; D018994:Myosin Light Chains / Q000378:metabolism; D016328:NF-kappa B / Q000502:physiology; D009929:Organ Size / Q000502:physiology; D009195:Peroxidase / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D010952:Plasma Substitutes / Q000494:pharmacology; D050796:STAT3 Transcription Factor / Q000502:physiology; D013152:Splanchnic Circulation / Q000502:physiology
chemical_list: D000077324:Crystalloid Solutions; D007552:Isotonic Solutions; D018994:Myosin Light Chains; D016328:NF-kappa B; D010952:Plasma Substitutes; D050796:STAT3 Transcription Factor; C494087:Stat3 protein, mouse; D009195:Peroxidase