Strain Specific Persistent Suppression of Visceral Pain Perception After Recovery From a Bout of Colitis

Abstract

Visceral pain is often experienced by patients with GI inflammation, and some studies suggest that such pain can persist after resolution of inflammation. Colitis was induced in male Wistar and Sprague‐Dawley (SD) rats via intrarectal administration of dinitrobenzene sulfonic acid (DNBS) in 50% ethanol, controls received saline only. At day 15, under general anesthesia, a balloon was inserted into the colon and distended (colo‐rectal distention; CRD), heart rate was recorded continuously. Cardioautonomic responses to CRD were analyzed and expressed as % change from the pre‐CRD heart rate. Colonic injury and inflammation were examined histologically and by measurement of tissue myeloperoxidase activity. By 15 days following DNBS administration, colitis had resolved. CRD caused a significant visceral pain response (bradycardia) in both strains of control rats. However, Wistar rats showed a significant suppression of pain response to CRD, whereas the response in SD rats remained the same after colitis. There was no difference in colonic compliance between control and DNBS groups or the two strains. Our results provide evidence of a strain‐dependent alteration in the pain response to CRD that persists after resolution of colitis, likely due to changes in autonomic sensory function induced by inflammation. Our results are consistent with the variability in pain perception seen in patients with GI inflammation.