一氧化氮在肝硬化腹水大鼠钠潴留中的作用研究

摘要

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cGMP含量，用电极法测定上述三组大鼠24 h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cGMP水平显著高于假手术组，24 h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cGMP水平，同时24 h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) in sodium retention of cirrhosis, NO-dependent cGMP concentration was measured by radioimmunoassay (RIA) method in plasma and homogenates of renal tissue of biliary cirrhotic rats with ascites (CIR) induced by bile duct ligation (BDL), cirrhotic rats with ascites treated with L-NAME (CIR-NAME), and sham-operating rats (SO). 24-h urinary sodium excretion in the three groups of the rats was determined by using electrode. The results showed that the concentration of cGMP in plasma and homogenates of renal tissue of CIR rats was significantly lower and urinary sodium excretion significantly lower than that in SO rats. By contrast, the administration of a low dose of L-NAME (0. 5 mg/kg per day) for one week to cirrhotic rats with ascites could significantly reduced the concentration of cGMP and obviously elevate the 24-h urinary sodium excretion. It was suggested that inhibition of nitric oxide synthase (NOS) for one week could increase the renal sodium excretion in cirrhotic rats with ascites. NO might participate in the pathogenesis of sodium retention in cirrhosis.