采用放免分析法测定了ＣＯＰＤ、ＣＰＨＤ患者急性发作期血浆中ＥＴ１含量及应用盐酸精氨酸治疗前后血浆ＥＴ１水平变化。结果提示，ＣＯＰＤ、ＣＰＨＤ急性发作期外周静脉血ＥＴ１水平较正常组显著升高（Ｐ＜０００１），且ＣＰＨＤ急性发作期ＥＴ１水平较ＣＯＰＤ患者显著增高（Ｐ＜０００１）。急性发作期患者ＥＴ１含量与ＰａＣＯ２呈显著正相关，与ＰａＯ２、ｐＨ值呈显著负相关。ＬＡｒｇ组和对照组治疗前血浆ＥＴ１含量无显著差异，而治疗后ＬＡｒｇ组ＥＴ１水平较对照组有显著降低（Ｐ＜０００１）。提示ＥＴ１可能参与了ＣＯＰＤ、ＣＰＨＤ的发病过程，测定血浆ＥＴ１的水平变化可望作为判定病情严重程度的一个指标。ＬＡｒｇ可能作为ＮＯ供体通过增加ＮＯ的生成而拮抗ＥＴ１的产生，有可能成为ＣＯＰＤ、ＣＰＨＤ治疗的一个新途径 Radioimmunoassay was used to determine the plasma levels of ET-1 in patients with COPD and CPHD during acute exacerbation and the plasma levels of ET-1 before and after treatment with arginine hydrochloride. The results suggest that COPD, CPHD acute exacerbation of peripheral venous blood ET 1 levels were significantly higher than the normal group (P <0001), and CPHD acute exacerbation of ET 1 levels were significantly higher than COPD patients (P <0  001 ). In patients with acute exacerbation of ET 1 content was significantly correlated with PaCO2, and PaO2, pH was significantly negatively correlated. L  Arg group and control group before treatment plasma ET  1 content was no significant difference, while L  Arg group ET  1 levels were significantly lower than the control group (P <0  001). Suggesting that ET 1 may be involved in the pathogenesis of COPD, CPHD, the determination of plasma levels of ET 1 is expected to be used as an indicator of the severity of the disease. L  Arg may serve as NO donors through the generation of NO to antagonize the production of ET  1, may be a new way of COPD, CPHD treatment