Ischemic-reperfusion injury (IRI) is thought to be caused by oxygen radicals. Nitric oxide (NO) also has been thought to play a key role in IRI. This experiment was designed to evaluate the effects of antioxidants and NO supplement on hepatic IRI. Male Sprague-Dawley rats were divided into five groups: a sham operation group, a group with IRI, and three groups with vitamin C combined with vitamin E (VC&VE), L-arginine and N(G)-nitro-L-arginine (NNLA) injected after IRI. IRI was induced by clamping of the porta hepatis for 30 minutes and then by declamping. To prevent mesenteric blood congestion, a porto-systemic shunt had been made four weeks before the portal clamping. Biochemical assays of TNF-alpha level and NO2- level in the blood, malondialdehyde level, catalase activity and NO synthase activity in the liver tissue were performed. The results were as follows: IRI increased the malondialdehyde level and exhausted the catalase activity remarkably. VC&VE lowered the malondialdehyde levels and protected against catalase exhaustion, but had no significant effect on the NO production. L-arginine had a definite antioxidant effect, which was much weaker than that of VC&VE. In conclusion, antioxidants and a supplement of NO protected the liver tissue against IRI
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