• Stacey D Moore-Olufemi, Hasan Xue, Bashir O Attuwaybi, Uwe Fischer, Y Harari, D H Oliver, Norman Weisbrodt, Steven J Allen, Frederick A Moore, Randolph Stewart, Glen A Laine, and Charles S Cox.
• 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.
• J Trauma. 2005 Feb 1;58(2):264-70.

BackgroundMesenteric 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.MethodsThe 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.ResultsVenous 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.ConclusionAcute 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.

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