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目的:探讨氧自由基代谢在慢性阻塞性肺疾病(COPD)发病机制中的作用。方法:采用生化、放射免疫方法,测定39例COPD患者血液MDA,SOD,ET-1,ACE,并进行血气和血流动力学参数测定。结果:COPD患者MDA水平均较正常对照组(C组)增高,而肺动脉高压组(B组)患者MDA又较非肺动脉高压组(A组)明显增高(F=25.30,P<0.01);B组患者SOD活性较A组和C组明显降低(F=4.56,P<0.05),所有COPD患者肺动脉血SOD均较桡动脉血和周围静脉血明显降低(F=6.33,P<0.01)。B组患者ET-1和ACE均较A组和C组明显增高(F=9.251～13.96,P<0.01);所有COPD患者肺动脉血ACE均较桡动脉血和周围静脉血明显增高(F=10.95,P<0.01)。肺动脉血中MDA与mPAP,PVRI呈正相关,与PaO2呈负相关;ET-1与mPAP,PVRI,TPRI呈正相关;多元回归分析显示MDA和ET-1分别作为独立因素影响mPAP,其中MDA对mPAP的影响力大于ET-1。结论:COPD患者体内常处在氧化反应增强,抗氧化能力降低的氧化胁迫状态。氧自由基通过直接损伤血管内皮细胞,导致内皮功能失调,参与肺动脉高压的形成和发展。
Objective: To investigate the role of oxygen free radical metabolism in the pathogenesis of chronic obstructive pulmonary disease (COPD). Methods: The biochemical and radioimmunoassay methods were used to determine the blood levels of MDA, SOD, ET-1 and ACE in 39 COPD patients and the blood gas and hemodynamic parameters were measured. Results: The levels of MDA in COPD patients were significantly higher than those in normal control group (C group), while those in pulmonary hypertension group (B group) were significantly higher than those in non-pulmonary hypertension group (F = 25.30, P <0.01) The activity of SOD in group A was significantly lower than that in group A and C (F = 4.56, P <0.05). The level of SOD in pulmonary arterial blood in all COPD patients was significantly lower than that in radial artery and peripheral venous blood (F = 6.33, P <0.01). ET-1 and ACE in group B were significantly higher than those in group A and C (F = 9.251-13.96, P <0.01); ACE in pulmonary arterial blood was significantly higher in all COPD patients than in radial artery and peripheral venous blood (F = 10.95 , P <0.01). Pulmonary arterial blood MDA was positively correlated with mPAP and PVRI and negatively correlated with PaO2. ET-1 was positively correlated with mPAP, PVRI and TPRI. Multivariate regression analysis showed that MDA and ET-1 affected mPAP as independent factors, Impact is greater than ET-1. CONCLUSIONS: COPD patients often have oxidative stress and oxidative stress with reduced antioxidant capacity. Oxygen free radicals through direct damage to vascular endothelial cells, leading to endothelial dysfunction, involved in the formation and development of pulmonary hypertension.