ACTIVE OXYGEN SPECIES IN FORMATION OF ACUTE GASTRIC-MUCOSAL LESIONS INDUCED BY THERMAL-INJURY IN RATS

Active oxygen species generated by circulating leukocytes and released from the gastric mucosa were measured in the process of acute gastric mucosal lesion formation after thermal injury in rats. Alterations of luminol-dependent chemiluminescence activities generated by leukocyte s obtained from the gastric vein and the inferior vena cava were appro ximately same. A decrease in chemiluminescence activity 15 min after t hermal injury and a significant increase in chemiluminescence activity 5 hr after thermal injury were observed in leukocytes from both veins . From 15 min to 12 hr after thermal injury, luciferin-dependent chemi luminescence activities were significantly higher than that of the con trol group. Oral administration of rebamipide resulted in decreased mu cosal lesion formation. Rebamipide, an antiulcer agent that protects t he mucosa from damage in various animal models decreased chemiluminesc ence activities only released from the gastric mucosa but not from cir culating leukocytes. These results suggest that two different pathways of active oxygen species formation may exist in the pathogenesis of a cute gastric mucosal lesions after thermal injury.