Visceral surface oxygen tension in experimental colitis in the rabbit.

The impairment of bowel healing that is characteristic of inflammatory bowel disease (IBD) is poorly understood. Because bowel healing is related to the adequacy of perfusion in other circumstances, we studied bowel surface oxygen tension (PSO2), which is related to bowel perfusion, in rabbits with IBD. Both cell-mediated (n = 17) and immune complex-mediated (n = 10) colitis caused marked attenuation of colon PSO2. Control (n = 13) left colon PSO2 was 36 +/- 5 (SEM) torr. In mild colitis, left colon PSO2 fell to 11 +/- 5 torr, and in severe colitis it fell to 4 +/- 1 torr (p less than 0.01 for each compared with control). These changes occurred irrespective of the mechanism of induction of colitis. Gastric and small intestinal PSO2 were unaffected. Hepatic and renal PSO2 were decreased in severe colitis only. The presence of decreased PSO2 was a better marker for the presence of IBD than was histologic evaluation. It is suggested that attenuation of PSO2 may be a marker for the physiologic activity of IBD. If this is so, PSO2 may prove a useful adjunct in the operative management of IBD.