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肝硬化普遍存在着高动力循环状态，一些血管扩张物质参与了这种异常状态的发生。为探讨扩血管物质一氧化氮在肝硬化时的水平及其产生机制，测定了３８例肝硬化患者及１５例正常对照者血浆中一氧化氮代谢产物ＮＯ２－／ＮＯ３－及内毒素、肿瘤坏死因子α（ＴＮＦα）、环磷酸鸟苷（ｃＧＭＰ）含量。结果发现，ＮＯ２－／ＮＯ３－水平较正常对照显著升高，与增多的内毒素、ＴＮＦα水平呈正相关，血中ＮＯ２－／ＮＯ３－水平随肝功能Ｃｈｉｌｄ－Ｐｕｇｈ分级增加而升高。提示肝硬化时，一氧化氮合成增加，且与内毒素、ＴＮＦα诱导有关，前者可能是肝硬化血液动力学紊乱等产生的重要原因。
Cirrhosis prevalence of hyperdynamic circulation, some vasodilators involved in the occurrence of this abnormal state. In order to investigate the level of vasoconstrictor nitric oxide in cirrhosis and its mechanism, the levels of nitric oxide metabolites NO2- / NO3- and endotoxin in plasma of 38 patients with cirrhosis and 15 normal controls were determined. Tumor necrosis Factor α (TNFα), cyclic guanosine monophosphate (cGMP) content. The results showed that the level of NO2- / NO3- was significantly higher than that of the normal control, positively correlated with the increased levels of endotoxin and TNFα, and the level of NO2- / NO3- was increased with the increase of Child-Pugh classification. Prompted cirrhosis, nitric oxide synthesis increased, and endotoxin, TNFα-induced, the former may be an important cause of cirrhosis and other hemodynamic disorders.