Mechanisms of increased intestinal [51Cr]EDTA absorption during experimental colitis in the rat.

Experimental colitis was induced in the rat, by ethanol-oxazolone injections into the distal colon, resulting in diarrhea together with edema, ulcers, and cell infiltration in the exposed colon. Colitic rats showed an elevated urinary recovery of the permeability marker [51Cr]EDTA after intragastric feeding, 19 +/- 10%, compared to 2.9 +/- 0.7% for control rats (P < 0.001). An increased retention of [51Cr]EDTA in the intestines and a decreased discharge in feces suggested an increased intestinal transit time in colitic rats. The in vitro permeability to [51Cr]EDTA and ovalbumin was not elevated in the severely inflamed distal colon, but was in the proximal, unaffected colon to ovalbumin (P < 0.05) and in the distal small intestine, to both [51Cr]EDTA (P < 0.01) and ovalbumin (P < 0.05), indicating that an inflammation in one part of the intestine could have permeability effects in other remote parts. In conclusion, the increased [51Cr]EDTA absorption in vivo during colitis was probably due to both an increased permeability and an increased intestinal transit time.