Adoptive transfer of naive CD4⁺ T-cells into lymphopenic mice induces chronic small and large bowel inflammation similar to Crohn's disease. Although much is now known regarding the immunopathology in this model of inflammatory bowel disease, virtually nothing is known about the microvascular hemodynamic changes during the induction and perpetuation of chronic gut inflammation. In this study, CD4⁺CD45RB^high T-cells obtained from healthy C57BL6 donor mice were transferred into lymphopenic recombinase activating gene-1 deficient (RAG knockout) mice, which induced small and large bowel inflammation. At various time points following reconstitution (3 days - 9 weeks), intravital microscopy was used to examine the microvessels in the submucosa of the ileum and proximal colon following infusion of fluorescently labeled platelets and injection of rhodamine 6G (to label leukocytes). Hemodynamic measurements and the extent of blood cell adhesion to the venular wall were compared to measurements in unreconstituted RAG knockout controls. In < 1 week following reconstitution, velocity and wall shear rate of the arterioles decreased by > 50% compared to controls, with this decrease also observed at 4-5 and 7-9 weeks post-reconstitution. At 7-9 weeks, arteriolar diameters were found to be ~15% larger than in controls, but despite this dilation, flow rates in the individual vessels were decreased by ~30%. Venular platelet and leukocyte adherence were not significantly elevated above controls; however, an association was found between platelet adherence and venular shear rate. In summary, significant decreases in arteriolar velocity and shear rates are observed in this model of chronic gut inflammation.