@entity1960 reduces short-circuit current response to inflammatory mediators in XXXX colonic mucosa.

@entity1 @entity32 @entity2544 @entity294 @entity1138 @entity1960 @entity841 @entity5015 @entity750 @entity1812 @entity35 @entity5402
Inflammatory mediators may contribute to the @entity294 associated with @entity1960 . Although the secretory action of such mediators is reported in normal tissue, there is little information regarding their effects on inflamed tissue. We examined the short-circuit current response (Isc) to these mediators, in @entity1138 (MC)-induced @entity1960 , a model with histological similarities to @entity1960 in @entity1 . @entity35 were injected once with MC (3.25 mg/kg, intraperitoneally) or vehicle. The colons were removed three and seven days later and mounted, devoid of muscularis, in Ussing chambers for measurement of Isc, @entity841 ( @entity841 ), and resistance (Rt). MC-treated @entity35 had @entity294 after three days, and microscopic studies revealed @entity32 . There were no significant differences in Rt, @entity841 , and Isc between control and MC-treated tissues at three and seven days. Maximal increases in Isc to @entity1812 , @entity5015 , @entity5402 , substance P, and @entity750 were depressed at three and/or seven days after MC. The Isc response to @entity2544 was not affected. Theophylline activates secretion through an intracellular mechanism; the other agonists act by interaction with epithelial cell membranes. Therefore, the mechanism for the decreased Isc may result from uncoupling of receptors to second-messenger systems or desensitization of receptor-linked secretory mechanisms.
