INTRACOLONIC RELEASE OF NITRIC-OXIDE DURING TRINITROBENZENE SULFONIC-ACID RAT COLITIS

Nitric oxide is thought to play an important role in modulating the in flammatory process. Recently an increase in the inducible form of nitr ic oxide synthase (iNOS) has been found in the rat trinitrobenzene sul fonic acid model of experimental colitis, and inhibition of nitric oxi de synthase activity resulted in an amelioration of tissue injury. The aim of our study was to evaluate in vivo intracolonic release of nitr ic oxide in this model of colitis Experimental colitis was induced in male Sprague-Dawley rats by a single intracolonic administration of tr initrobenzene sulfonic acid. Nitrite levels were determined in rectal dialysates by HPLC. The tissue myeloperoxidase and iNOS and the lumina l leukotriene B-4 were also measured. Nitrite levels were significantl y increased in rectal dialysates during colitis and correlated signifi cantly with tissue myeloperoxidase and iNOS activity. The correlation between nitrite dialysate levels and wall iNOS activity confirms that nitrite in dialysates is produced by inflammatory cells and not by col onic bacterial flora, Determination of nitrite levels in rectal dialys ates seems a valuable method to monitor colonic inflammation in rat tr initrobenzene sulfonic acid colitis.