Effect of ischemia on the canine large bowel: a comparison with the small intestine.

Mucosal injury caused by ischemia and reperfusion has been well documented with the small intestine, but little is known about the colon. In the present study, the effect of warm and cold ischemia on the canine colon was studied and compared to that on the small intestine. After in situ flushing, the small intestine and the colon from six beagle dogs were removed and stored for 0.5, 1.5, and 3 hr at 37 degrees C (warm ischemia) or for 1, 6, 12, 24, 36, and 48 hr at 4 degrees C (cold ischemia). Electrophysiology, permeability, biochemistry, and histopathology of the specimens at each ischemic period and after reperfusion in the Ussing chamber were determined. Warm and cold ischemia induced duration-dependent suppression of electrophysiology in both organs, but the colonic mucosa retained higher activity of absorptive enterocytes and cryptic cells than the small intestine. Only the colon showed increased permeability of FITC-conjugated Dextran from the mucosal surface to the submucosal layer after prolonged ischemia. Changes in adenine nucleotides and purine catabolites were not markedly different between the organs. Histopathologic abnormalities during ischemia and after reperfusion were more serious with the small intestine than with the colon. Compared to warm ischemia, hypothermia lessened or delayed these morphofunctional derangements in both organs, which became universally worsened after reperfusion. Colonic mucosa receives morphofunctional derangements from ischemia and reperfusion, but the severity of the damage was much less severe in the colon than in the small intestine.