Detection of O-2 Generated in the Rat Gastric Mucosa In Situ during Reperfusion Following Ischemia

The objectives of the present investigation were to examine the effect of ischemia and reperfusion on superoxide anion (O-2) generation, leukocyte infiltration, edema, and erosion (injury) in the rat gastric mucosa. Ischemia of 5-, 15-, and 30-min duration was applied to the gastric tissue followed by 2.5h of reperfusion. O-2 generation in the gastric mucosa in situ during reperfusion was measured by use of a highly sensitive luminescence reagent, 2-methyl-6-phenyl-3, 7-dihydroimidazo [1.2-α] pyrazin-3-one (CLA) and a photon counting technique. Leukocyte infiltration, edema, and erosion were determined by examining gastric mucosa tissue post-reperfusion. O-2 generation, the extent of edema, and erosion all increased with the duration of Ischemia, but leukocyte infiltration was maximum after an ischemia of 15-min duration, with a corresponding reperfusion period of 15min. Administration of an O-2 scavenger, superoxide dismutase (SOD), effectively abolished O-2 detection and markedly reduced the extent of edema but was virtually ineffective on leukocyte infiltration and mucosal erosion. Similarly, the xanthine oxidase inhibitor allopurinol markedly supressed O-2 detection, edema, and mucosal erosion, but was ineffective against leukocyte infiltration into the mucosal tissue. These observations suggest that more than one mechanism contributes to tissue injury induced by ischemia and reperfusion in this model.