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为探讨血管活性物质一氧化氮 (NO)在肝硬化钠潴留中的作用 ,采用放射性免疫法测定胆管结扎 (BDL)诱导的胆汁性肝硬化腹水组 (CIR)和肝硬化腹水给药组 (CIR- NAME)及假手术组 (SO)大鼠血浆和肾组织匀浆中 NO依赖性 c GMP含量 ,用电极法测定上述三组大鼠 2 4h尿钠排泄量。结果显示 :肝硬化腹水大鼠血浆和肾组织匀浆中c GMP水平显著高于假手术组 ,2 4h尿钠排泄量则显著低于假手术组。而持续给予小剂量 [(0 .5 mg/ (kg· d) ) ]NO合酶 (NOS)抑制剂 L- NAME达一周 ,能显著降低肝硬化腹水大鼠体内 c GMP水平 ,同时 2 4h尿钠排泄量明显增加。从而提示 :使一氧化氮合酶 (NOS)抑制达一周可增加肝硬化腹水大鼠肾钠排泄量 ,推测 NO途径可能参与了肝硬化钠潴留的发生机制
To investigate the role of nitric oxide (NO), a vascular active substance, in cirrhosis retention, we used radioimmunoassay to determine the level of CIR in biliary cirrhosis induced by biliary duct ligation (BDL) and CIR - NAME) and sham operation group (SO), respectively. The levels of urinary sodium excretion in 24 hours were measured by electrode method. The results showed that the levels of c GMP in plasma and kidney homogenate of cirrhotic rats were significantly higher than those in sham-operation group, while the levels of urinary sodium excretion in 24 h were significantly lower than those in sham operation group. However, continuous administration of low-dose [(0.5 mg / (kg · d))] N-synthetase NOS inhibitor L-NAME for one week significantly reduced c GMP levels in cirrhotic ascites rats and 24 h urine Sodium excretion increased significantly. This suggests that inhibition of nitric oxide synthase (NOS) for up to one week increases renal sodium excretion in cirrhotic rats, suggesting that the NO pathway may be involved in the pathogenesis of cirrhosis