吡那地尔对慢性阻塞性肺疾病肺动脉高压患者疗效的临床研究

Clinical study of the effects of pinacidil on pulmonary hypertention in chronic obstructive pulmonary disease

目的评价吡那地尔(Pin)对慢性阻塞性肺疾病(COPD)肺动脉高压(PH)患者的疗效及其作用机制。方法将2009年1月-2012年1月诊治的COPD合并PH的患者178例,随机分为治疗组(A组)和对照组(B组)各89例。B组给予常规治疗,A组在常规治疗的基础上加用吡那地尔缓释胶囊25mg,2次/d,疗程4周,观察治疗前后两组肺动脉压收缩压(PAPs)、内皮素-1(ET-1)、动脉血氧分压(PaO2)、动脉血二氧化碳分压(PaCO2)、1s用力呼气容积占预计值百分比(FEV1%pred)、第1s用力呼气容积占用力肺活量百分比(FEV1/FVC%)、6min步行距离(6MWD)及血压(BP)。结果A组治疗后PAPs、ET-1、PaCO2、及BP均有明显下降,与B组治疗后比较差异有统计学意义(P<0.05);而PaO2、FEV1%Pred、FEV1/FVC%及6MWD有显著提高,与B组治疗后比较差异有统计学意义(P<0.05)。结论Pin通过降低血浆ET-1浓度降低肺动脉压力、改善患者肺功能及提高生活质量。

Objeetive To evaluate the effect and mechanism of Pinacidil（Pin） treatment in patients with chronic obstructive pulmonary disease （COPD） combining with pulmonary hypertension （PH）. Methods 178 patients with COPD combining with PH from January 2009 to January 2012 were assigned randomly to two guoups： treatment group （group A, n=89）and control group （group B,n=89）.Group B was given conventional treatment.Patients in group A were given with pinacidil sustained-release cap- sules 25mg twice daily for 4 weeks besides the treatment on group B.Before and after treatment,the two groups of pulmonary artery systolic pressure （PAPs）,endothilin-1 （ET-1）,arterial oxygen pressure （PaO2）,arterial partial pressure of carbon dioxide（PaCO2）,ls forced expiratory volume in percentage of predicted value percentage （FEVl%pred）,second forced expiratory volume occupied by the percentage of vital capacity （FEV1/FVC%）,6min walk distance （6MWD）and blood pressure （BP）were measured.Results The PAPs,ET-1,PaCO2 and BP of group A after treatment was significantly decreased, compared with those of group B after treatment, there were statistically significant difference among them（P〈0.05 ,〈0.01, 〈0.05, 〈0.01）.While the PaO2,FEVI% Pred,FEV1/FVC% and 6MWD of group A after treatment was improved significantly, compared with those of group B after treatment there were sta- tistically significant difference among them （P〈0.05,〈0.01, 〈0.05, 〈0.01）.Conclusion Pinacidil reduce pulmonary artery pressure by lowering the plasma concentration of ET-1 and improve patients lung function and quality of life.