慢性阻塞性肺疾病患者氧自由基代谢对肺血流动力学的影响

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.

Effects of oxygen freeradical metabolism on pulmonary hemodynamics in patients with chronic obstructivepulmonary disease

AIM:To investigate the effects of oxygen free radical metabolism on pathogenic mechanism of chronic obstructive pulmonary disease(COPD). METHODS: Biochemistry tests and radioimmunoassay were performed in 39 COPD patients,and the blood levels of malondialdehyde(MDA),superoxide dismutase(SOD),endothelins-1(ET-1),angiotensin-converting enzyme(ACE),and parameters of blood gases and hemodynamics were measured. RESULTS: The level of MDA of COPD patients was higher than that of the controls(group C).In addition,the patients with pulmonary hypertension (group B)had a higher level of MDA than the patients without pulmonary hypertension(group A)(F=25.30,P< 0.01);SOD activity of the group B was much lower than that of the group A and C(F=4.56,P< 0.05),which was significantly decreased in patient pulmonary artery blood compared with in radial artery and peripheral vein blood(F=6.33,P<0.01). The levels of ET-1 and ACE in the group B were clearly higher than those of the group A and C(F=9.251－ 13.96,P< 0.01);the level of ACE in pulmonary artery was higher than that in radial artery and peripheral vein (F=10.95,P< 0.01).The level of MDA in pulmonary artery was positively correlated with mean pulmonary artery pressure(mPAP) and pulmonary resistance index (PVRI) while was negatively correlated with PaO2; the level of ET-1 was positively correlated with mPAP,PVRI and total pulmonary resistance index(TPRI).Multiple regression analysis showed that MDA and ET-1 could influence mPAP as independent factors,and the effect of MDA was larger than that of ET-1. CONCLUSION: There is an increased oxidative stress and decreased anti-oxidative ability in COPD patients.The development of pulmonary hypertension is closely related to the oxygen free radicals induced direct injury of endotheliocyte.