title: Resuscitation-induced gut edema and intestinal dysfunction.
abstract: BACKGROUND
  Mesenteric venous hypertension and subsequent gut edema play a pivotal role in the development of intra-abdominal hypertension. Although gut edema is one cause of intra-abdominal hypertension, its impact on gut function is unknown. The purpose of this study was to create a model of acute hydrostatic gut edema and to evaluate its effect on gut motility and barrier function.
  
  
  METHODS
  The first study, group A, evaluated the effect of gut edema on transit over time using 20 mL/kg 0.9% saline. The second study, group B, focused on the 12-hour time period using 80 mL/kg 0.9% saline. Rats were randomized to superior mesenteric vein partial occlusion (venous hypertension) or sham surgery. At 6, 12, and 24 hours, group A underwent intestinal transit and tissue water weight measurements. At 12 hours, group B underwent tissue water, transit, ileal permeability and resistance, lactate and myeloperoxidase activity, and mucosal injury measurements.
  
  
  RESULTS
  Venous hypertension with fluid resuscitation caused acute hydrostatic gut edema, delayed intestinal transit, increased mucosal permeability to macromolecules, and decreased tissue resistance over time. Mucosal injury was minimal in mesenteric venous hypertension.
  
  
  CONCLUSIONS
  Acute mesenteric venous hypertension and resuscitation-induced gut edema, in the absence of ischemia/reperfusion injury, is associated with delayed intestinal transit and altered gut barrier function.
authors.affiliation: Department of Surgery, University of Texas-Houston Medical School, Houston, and The Michael E. DeBakey Institute, Texas A and M University, College Station, TX 77030, USA.
authors.forename: Stacey D
authors.initials: SD
authors.lastname: Moore-Olufemi
authors.forename: Hasan
authors.initials: H
authors.lastname: Xue
authors.forename: Bashir O
authors.initials: BO
authors.lastname: Attuwaybi
authors.forename: Uwe
authors.initials: U
authors.lastname: Fischer
authors.forename: Y
authors.initials: Y
authors.lastname: Harari
authors.forename: D H
authors.initials: DH
authors.lastname: Oliver
authors.forename: Norman
authors.initials: N
authors.lastname: Weisbrodt
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Allen
authors.forename: Frederick A
authors.initials: FA
authors.lastname: Moore
authors.forename: Randolph
authors.initials: R
authors.lastname: Stewart
authors.forename: Glen A
authors.initials: GA
authors.lastname: Laine
authors.forename: Charles S
authors.initials: CS
authors.lastname: Cox
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004487:Edema / Q000503:physiopathology; D005772:Gastrointestinal Transit; D007077:Ileal Diseases / Q000201:enzymology / Q000503:physiopathology*; D008297:Male; D009195:Peroxidase / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000517:prevention & control*; D012151:Resuscitation / Q000379:methods*; D012771:Shock, Hemorrhagic / Q000628:therapy; D012965:Sodium Chloride / Q000008:administration & dosage*
chemical_list: D012965:Sodium Chloride; D009195:Peroxidase