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利用四氯化碳加苯巴比妥诱导鼠肝硬化腹水模型,纵向、动态检测模型形成过程中肝功能、血浆心钠素(ANP)的变化趋势及其与钠排量的关系。结果显示:随肝脏结构损伤,肝硬化及腹水的形成,肝功能呈进行性恶化,ANP 呈进行性升高,第9周显著高于对照组(分别为264.9±41.6、197.5±39.5 ng/L,P<0.05),腹水形成后 ANP 仍维持在较高水平。尿钠排量随 ANP 升高反而呈进行性下降,于第9周及腹水形成后显著低于对照组(分别为0.80±0.22、1.43±0.26 mmol/24 h,P<0.05)。提示:①肝硬化腹水形成过程中不存在 ANP 释放缺陷;②与(?)钠激素相比,ANP 在调节肝硬化钠平衡中居次要地位。
The use of carbon tetrachloride and phenobarbital to induce murine cirrhosis model of liver cirrhosis, longitudinal and dynamic detection of liver function in the process of model formation, plasma ANP trends and its relationship with sodium output. The results showed that with the structural damage of the liver, cirrhosis and ascites, the liver function progressed worsened and ANP increased progressively, which was significantly higher than that of the control group at the 9th week (264.9 ± 41.6 and 197.5 ± 39.5 ng / L , P <0.05), ANP still maintained at a high level after the formation of ascites. However, the urinary sodium excretion decreased with the increase of ANP, but decreased significantly after 9 weeks and ascites (0.80 ± 0.22, 1.43 ± 0.26 mmol / 24 h, P <0.05, respectively). Tip: ① cirrhosis of the formation of ascites ANP release defect does not exist; ② and (?) Sodium compared to the regulation of hepatic sodium balance ANP in the secondary position.