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INTESTINAL ISCHEMIA: REPERFUSION-MEDIATED INCREASE IN HYDROXYL FREE RADICAL FORMATION AS REPORTED BY SALICYLATE HYDROXYLATION.

Rose, Stefan; Floyd, Robert A.; Eneff, Kent; Bühren, V.; Massion, Walter

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Abstract

Oxygen free radicals may play a pivotal role in the development of the shock-induced inflammatory response syndrome. Hydroxyl free radicals (OH) react with salicylate (SA) to form 2,5- and 2,3-dihydroxybenzoic acid (DHBA) products. We utilized salicylate hydroxylation to investigate [middle dot]OH formation during intestinal ischemia/reperfusion injury in male Sprague-Dawley rats. After administering salicylate, the superior mesenteric artery was occluded for 45 min and then allowed to reperfuse for 90 min after declamping. No significant changes in plasma 2,3-and 2,5-DHBA/SA ratios were observed in sham-operated or in animals given intestinal ischemia without reperfusion. A significant increase (p < .05) in arterial, venous, and portal venous 2,5-DHBA/SA ratios occurred 5 min after reperfusion. This increase was prevented by allopurinol as well as by dimethylthiourea ([middle dot]OH scavenger) pretreatment. 2,3-DHBA was significantly increased (p < .05) in venous and portal venous blood after 30 min of reperfusion, but was not detectable in plasma of allopurinol-and dimethylthiourea-treated rats. These results indicate that hydroxyl free radical formation as reported by SA hydroxylation appears to be important in intestinal ischemia/reperfusion-related tissue injury.

(C)1994The Shock Society

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