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AIM: To investigate the effect of inducible nitric oxide synthase (iNOS) inhibitor animoguanidine (AG) during ischemia/reperfusion (I/R) in rat pancreas. METHODS: The models of sham-operation and pancreas ischemia were established in rats. The splenic artery of rats in I/R group was occluded reversibly by microsurgical clip for 30 minutes, and the animals were killed after 2, 4, 6, 12, or 24 hours of reperfusion. Aminoguanidine was given to the rats in AG group (40, 60, 80 mg/kg; iv). Rats in control group received saline only. The serum nitric oxide (NO) level and amylase activity were detetermined with nitrate reductase and iodine-starch chromatometry. Pancreas constitutive NOS (cNOS) and iNOS activities were measured using NOS Test Kit. Pancreas sections were evaluated by light microscopy after HE and immunohistochemistry staining. RESULTS: In I/R group, serum NO level and amylase activity were increased significantly after 4-hour reperfusion. The NO level reached the peak and the amylase activity began to rise at 4 hour. After the administration of aminoguanidine (80 mg/kg), the NO level and amylase activity became much lower than those in the I/R group (P <0.01). After 4-hour reperfusion, tissue iNOS activity was increased significantly in I/R group, but remained normal in AG group (P <0.01). Six, twelve, and twenty-four hours after reperfusion, pancreas injury was observed in I/R group, but no siginificant changes occurred in pancreas after animoguanidine (80 mg/kg) administration. Four hours after reperfusion, the positive rate of iNOS in the specimens from I/R group was significantly higher than that in AG (80 mg/kg) group (439±127 vs 33±4, P <0.01). The activity of cNOS showed no significant difference between

Protcetive effect of iNOS inhibitor on pancreas ischemia/reperfusion injury in rats