阿托伐他汀对肺心病患者血清中8-iso-PG水平的影响

Effect of atorvastatin on serum 8-iso-PG level in patients with chronic pulmonary heart disease

目的探讨阿托伐他汀对慢性肺源性心脏病患者血清中8-异前列腺素的影响及可能机制。方法选择南通大学第二附属医院急诊科和呼吸科住院的45例慢性肺源性心脏病患者,随机分成阿托伐他汀治疗组(23例)和常规治疗组(22例),常规治疗组予吸氧、抗感染、止咳化痰、平喘等对症治疗,阿托伐他汀治疗组在此基础上加用阿托伐他汀20 mg口服,每晚一次,疗程6个月。分别于治疗前后行超声心动图、6分钟步行距离(6MWD)、动脉血气分析检查,同步收集血清标本,采用酶联免疫吸附方法(ELISA)方法检测血清中8-异前列腺素(8-iso-PG)。比较阿托伐他汀治疗组与常规治疗组治疗前后的肺动脉压力、动脉血气分析、6MWD、血清中8-iso-PG水平,分析临床指标和各个检测指标的相关性。结果①治疗前,两组血清中8-isoPG水平无明显差异(P>0.05)。在治疗后,两组血清中8-iso-PG水平较前下降,P<0.05,但阿托伐他汀治疗组较常规治疗组降低更明显(P<0.05)。②在治疗后,阿托伐他汀治疗组肺动脉压(PASP)较前明显降低,动脉血氧分压(PaO2)、6-MWD较前明显增高;而常规治疗组无明显改变,P均>0.05,两组比较有显著差异(P<0.05)。结论阿托伐他汀能降低慢性肺源性心脏病患者肺动脉压力,提高动脉血氧分压,改善活动耐力,其机制可能与抑制炎症反应和氧化应激有关。

Objective To investigate the effect and the possible mechanism of atorvastatin on serum 8-isoprostane in patients with chronic pulmonary heart disease. Methods 45 patients with chronic pulmonary heart disease were randomly divided into two groups： the atorvastatin treatment group（ n = 23） and the conventional treatment group（ n = 22）. The conventional treatment group received conventional therapy according to chronic pulmonary heart disease,and the atorvastatin treatment group received extra atorvastatin 20 mg /day. They were treated for 6 months respectively. Before and after the treatment,their lung function,arterial blood gases,echocardiography,6MWD,liver and kidney function and serum samples were analyzed. The level of 8-isoprostane（ 8-iso-PG） in serum was measured by enzyme-linked immunosorbent assay（ ELISA）. The relationships were analyzed between the clinical parameters and detective indicators. Results ① Before the treatment,there was no significant difference in serum 8-iso-PG concentrations between the two groups（ P〉0. 05）. After the treatment,the level of 8-iso-PG in serum both decreased in the two groups（ P〈0. 05）,but the decline was more obviously in the atorvastatin treatment group than in the control group（ P〈0. 05）. ② 6 months after the treatment,PASP significantly decreased in the atorvastatin treatment group and PaO2and 6MWD increased significantly（ P〈0. 01）. However,there was no significant difference in the control group（ P〉0. 05）. Conclusion Atorvastatin can significantly reduce PASP,improve arterial oxygen partial pressure and exercise tolerance of chronic pulmonary heart disease. The mechanism may be that atorvastatin can inhibit the inflammatory reaction,oxidative stress of system and local respiratory tracts.