We have previously shown that PGI₂ and PGE₂ have a synergistic role in restoring electrical transepithelial resistance (R) in ischemia-injured porcine ileum via the second messengers Ca²⁺ and cAMP. Because Ca²⁺ and cAMP stimulate Cl secretion, we assessed the role of PG-induced Cl secretion in recovery of R. Mucosa from porcine ileum subjected to ischemia for 45 min was mounted in Ussing chambers and bathed in indomethacin and Ringer solution. Addition of PGs stimulated a twofold increase in R, which was preceded by elevations in short-circuit current (increase of 25 µA/cm²). The PG-induced effect on R was partially inhibited with bumetanide, an inhibitor of Cl secretion. The remaining elevations in R were similar in magnitude to those induced in ischemic tissues by amiloride, an inhibitor of Na⁺ absorption. Treatment with 10⁴ M 8-bromo-cGMP or 300 mosM mucosal urea resulted in elevations in R similar to those attained with PG treatment. PGs signal recovery of R via induction of Cl secretion and inhibition of Na⁺ absorption, possibly by establishing a transmucosal osmotic gradient.

tight junction; ischemia; mucosa

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