一氧化氮胰腺保护作用与巯基物质和氧自由基的关系

目的　探讨内源性一氧化氮 (NO)对大鼠急性坏死性胰腺炎的作用及其与巯基物质和脂质过氧化之间的关系。　方法　以 5 %牛磺胆酸钠溶液胰胆管注射 (1ml/kg)制成大鼠急性坏死性胰腺炎模型 ,以工具药L 硝基精氨酸 (L NNA)为内源性NO的阻断剂 ,观察内源性NO对胰腺损伤程度、血清淀粉酶浓度、胰腺组织内巯基物质含量和脂质过氧化终产物丙二醛 (MDA)含量的影响。　结果　牛磺胆酸钠胰胆管注射可造成胰腺组织明显的水肿和坏死 ,部分 (2 / 7)发生胰腺实质内出血 ;血清淀粉酶浓度显著升高 ,胰腺组织巯基物质含量降低 ,MDA含量增加 (1 2 5± 0 2 8)nmol/mg蛋白质vs.(0 5± 0 0 3)nmol/mg蛋白质 ,P <0 0 5 ]。以L NNA(12 5mg/kg)阻断内源性NO ,可明显加重胰腺组织坏死 ,胰腺实质内出血率增加 (10 / 12 ,83 3 % ) ,并血清淀粉酶浓度进一步升高 ,胰腺组织MDA含量进一步增加 (3 0± 0 40 )nmol/mg蛋白质vs.(1 2 5± 0 2 8)nmol/mg蛋白质 ,P <0 0 5 ]。但对胰腺组织内巯基物质的含量没有影响。　结论　内源性NO具有胰腺保护作用 ,其保护机制可能与抗氧自由基有关。巯基物质可能不参与NO的胰腺保护机制。

Protective effect of nitric oxide on pancreas and its relation to sulfhydryl compounds and oxygen free radicals

OBJECTIVE: To investigate the effect of endogenous nitric oxide (NO) on acute necrosis pancreatitis in rats and its relation to sulfhydryl compounds and lipid peroxidation. METHODS: Acute necrosis pancreatitis in rats was induced by retrograde sodium taurocholate (5%) infusion into the pancreatobiliary duct (1 ml/kg body weight), and N(G)-nitro-L-arginine (L-NNA) was used as the inhibitor of endogenous NO. The effect of endogenous NO on pancreatic injury, serum amylase level, the pancreatic tissue levels of sulfhydryl compounds, and malonaldehyde (MDA, the end product of lipid peroxidation) was evaluated, respectively. RESULTS: Sodium taurocholate administration induced evident pancreatic tissue edema and acinar necrosis, and intrapancreatic hemorrhage occurred in 2/7 rats. Both serum amylase and tissue MDA (1.25 +/- 0.28) nmol/mg x pr vs. (0.5 +/- 0.03) nmol/mg x pr, P < 0.05] were significantly increased, but tissue sulfhydryl compounds were decreased markedly. Pretreatment with the NO inhibitor, L-NNA (12.5 mg/kg body weight), significantly intensified acinar necrosis and increased the intrapancreatic hemorrhage (10/12). L-NNA also resulted in a further increase of serum amylase and tissue MDA (3.0 +/- 0.40) vs. (1.25 +/- 0.28) nmol/mg x pr, P < 0.05], but it had no effect on the tissue sulfhydryl compounds. CONCLUSION: Endogenous NO has the effect of pancreatic protection, and its antioxidation may be responsible, at least in part, for the protective mechanisms. Sulfhydryl compounds may not be involved in NO's pancreatic protection mechanisms.