The role of nitric oxide in the gastric acid secretion induced by ischemia-reperfusion in the pylorus-ligated rat

In a rat model of the ischemia-reperfusion with pylorus ligation, gastric u lcer was formed, although gastric acid secretion was reduced. When the poly morphonuclear leukocytes were inactivated in advance, gastric ulcer was not formed, but acid secretion was increased, indicating that gastric acid is not a cause of the ulcer formation in this model. The mechanism of gastric acid suppression accompanied by ischemia-reperfusion was examined in relati on to the role of oxygen-free radicals in this rat model. Prior administrat ion of superoxide dismutase did not modulate acid secretion, but N-nitro-L- arginine methyl ester (L-NAME) increased acid secretion. The action of L-NA ME was antagonized specifically by L-arginine, but not by D-arginine. S-nit roso-N-acetylpenicillamine did not inhibit basal acid secretion but antagon ized the action of L-NAME. Aminoguanidine increased significantly the gastr ic acid output that was suppressed by ischemia-reperfusion. When polymorpho nuclear leukocytes were inactivated by treatment with their antibody, the g astric acid output recovered to the level in the pylorus-ligated rat withou t ischemia-reperfusion. These results suggested that nitric oxide (NO) prod uced by the infiltrated polymorphonuclear leukocytes plays an important rol e in the suppression of acid secretion induced by ischemia-reperfusion. (C) 2001 Elsevier Science B.V. All rights reserved.