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目的探讨一氧化氮（ＮＯ）在肝硬变低蛋白血症中的作用。方法利用硫代乙酰胺（ＴＡＡ）腹腔注射大鼠诱导肝功能的变化，并用辅酶Ⅱ（ＮＡＤＰＨ）硫辛酰胺脱氢酶组织化学法显示不同肝功能时期肝脏一氧化氮合成酶（ＮＯＳ）的分布。结果正常鼠肝脏ＮＯＳ染色阴性；大鼠肝功能异常但无低蛋白血症时，肝小叶周边有少量散在的ＮＯＳ阳性细胞，至肝硬变有明显低蛋白血症时，假小叶内肝细胞均为ＮＯＳ染色阳性；停止注射ＴＡＡ４周后，大鼠肝功能逐渐恢复，但仍有低蛋白血症，此时假小叶内肝细胞仍为ＮＯＳ阳性，仅染色稍浅于肝功能明显异常时。结论肝硬变时肝细胞内ＮＯＳ被激活而产生ＮＯ，后者通过抑制肝细胞合成蛋白质而可能参与肝硬变时低蛋白血症的形成。
Objective To investigate the role of nitric oxide (NO) in cirrhosis with hypoproteinemia. Methods The hepatic function was induced by intraperitoneal injection of thioacetamide (TAA) in rats. The distribution of hepatic nitric oxide synthase (NOS) in different periods of liver function was detected by NADPH lipoamide dehydrogenase histochemical method . Results NOS staining in normal mice was negative. In rats with abnormal liver function but without hypoproteinemia, there were a few scattered NOS positive cells around hepatic lobule. When hepatic cirrhosis had hypoproteinemia, Positive for NOS staining. After 4 weeks of TAA injection, rat liver function gradually recovered but hypoalbuminemia was still present. In this case, the intrahepatic lobule hepatocytes were still positive for NOS, and only the staining was slightly lighter than when the liver function was obviously abnormal. Conclusion NOS is activated in liver cells to produce NO. The latter may be involved in the formation of hypoproteinemia in liver cirrhosis by inhibiting the synthesis of proteins in liver cells.