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<p>Increased visceral pain is often seen in patients with gastrointestinal (GI) inflammation. Some studies, however, have suggested that such pain may persist after resolution of damage or inflammation. Despite the debilitating pain associated with GI inflammation, and its significant impact on affected individuals, few studies have addressed this issue. We hypothesized that altered visceral pain responses would persist after resolution of a bout of colitis in an animal model of colitis. We studied the pain responses to colorectal distention in Wistar rats with dinitrobenzene sulfonic acid (DNBS)-induced colitis, using changes in heart rate as an index of pain. Colonic inflammation had resolved by day 15 after DNBS administration. The assessment of colonic inflammation was based on histological scores, colonic tissue pro-inflammatory cytokine levels and myleoperoxidase activity. Rats examined at 15 days post-DNBS administration exhibited diminished pain responses to colorectal distention as compared to healthy rats. This was associated with significant increases in colonic tissue levels of IL-4 and IL-10 as compared to healthy rats, indicating a possible role for these anti-inflammatory cytokines in counteracting the generation of pain and hyperalgesia. We also studied the effects of hydrogen sulfide (H2S) in our animal model, by administering inhibitors of two of the key enzymes involved in the production of H2S. Our results demonstrated that inhibition of H2S production did not significantly alter the pain responses observed in rats at 15 days post-DNBS administration. In summary, our results demonstrate altered autonomic responses to colorectal distension following resolution of colitis. Further research on the role of anti-inflammatory cytokines and H2S may help to determine the mechanism underlying this effect.</p> / Master of Science (MSc)