目的探讨肝硬变患者血氧变化及其发生机制．方法肝硬变患者６６例，应用血气分析仪测定其动脉血氧分压（ＰａＯ２）及氧饱和度（ＳａＯ２），其中肝炎后肝硬变６２例，酒精性肝硬变１例，血吸虫性肝硬变１例，原因不明肝硬变２例，肝功能ＣｈｉｌｄＡ级８例，Ｂ级３５例，Ｃ级２３例．选择同期１４例正常人作对照．结果肝硬变组平均ＰａＯ２为１１１３ｋＰａ±０１９ｋＰａ，ＳａＯ２为９７２２％±０１５％，正常对照组动脉血ＰａＯ２为１３１３ｋＰａ±０３６ｋＰａ，ＳａＯ２为９８０７％±０２５％，两者比较差异明显（Ｐ＜００１）．肝硬变患者ＰａＯ２，ＳａＯ２降低与门静脉内径，蜘蛛痣有关，与肝功能Ｃｈｉｌｄ分级，ＡＬＴ，胆碱酯酶无关，也与胸腔积液无关．结论肝硬变存在低氧血症，发生主要在于肺内血管扩张． Objective To investigate the changes of blood oxygenation in cirrhotic patients and its mechanism. Methods Sixty-six patients with cirrhosis were included. PaO2 and SaO2 were determined by blood gas analyzer. Among them, 62 cases were posthepatitic cirrhosis, 1 case was alcoholic cirrhosis, 1 case of cirrhosis, 2 cases of unknown liver cirrhosis, 8 cases of ChildA grade of liver function, 35 cases of grade B and 23 cases of grade C. Select the same period 14 cases of normal controls. Results The mean PaO2 of cirrhotic group was 1113kPa ± 019kPa and SaO2 was 9722% ± 015%. The arterial blood PaO2 of cirrhosis group was 1313kPa ± 036kPa, SaO2 was 9807% ± 0  25%, the difference between the two was significant (P <0  01). PaO2, SaO2 in patients with cirrhosis and portal vein diameter, spider nevus related, and liver function Child classification, ALT, cholinesterase has nothing to do, but also has nothing to do with pleural effusion. Conclusions There is hypoxemia in liver cirrhosis, which mainly results from the expansion of pulmonary blood vessels.