Intra-abdominal hypertension leading to abdominal compartment syndrome complicates trauma resuscitation. The purpose of this study was to determine the effect of primary (1) and secondary (2) intra-abdominal hypertension (IAH) on hemodynamics, intestinal fluid balance, and mesenteric lymph flow. Anesthetized dogs were instrumented with vascular catheters, intra-abdominal manometer, and mesenteric lymphatic fistulae. 1 IAH was created by infusing 0.9% saline into the peritoneal cavity to increase abdominal pressure. 2 IAH was created by elevating the inferior vena cava (IVC) pressure between 20 and 25 mmHg and crystalloid resuscitation to create intestinal edema to induce IAH. At baseline and at 30-min intervals, hemodynamics, lymph flow (Q L), IVC, and intra-abdominal pressures were measured. Tissue water was determined using microgravimetry to assess gut edema. Results are reported as mean±SEM, with n= 7-8 dogs per group. 1 IAH significantly increased CVP and decreased Q L. 1 IAH stopped mesenteric Q L, thus transvascular fluid flux necessarily exceeded Q L, contributing to gut edema formation. 2 IAH significantly increased CVP and Q L. 2 IAH increased Q L despite elevated IAP. Interstitial protein washdown maintained the plasma-to-interstitial oncotic gradient, thus increased transvascular fluid flux was due principally to increased capillary pressure. Transvascular fluid flux exceeded Q L as manifested by increasing gut tissue water as Q L plateaued. Modest elevations in IAP significantly affect mesenteric Q L and the development of gut edema. The principle of early abdominal decompression to reduce mesenteric/IVC venous hypertension and capillary pressure is supported by these data.