国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2013年
11期
819-824
,共6页
邱海艳%何海艳%马航%陶一江
邱海豔%何海豔%馬航%陶一江
구해염%하해염%마항%도일강
阿托伐他汀%慢性阻塞性肺疾病%肺动脉高压%呼出气冷凝液%高敏C-反应蛋白%肿瘤坏死因子-α
阿託伐他汀%慢性阻塞性肺疾病%肺動脈高壓%呼齣氣冷凝液%高敏C-反應蛋白%腫瘤壞死因子-α
아탁벌타정%만성조새성폐질병%폐동맥고압%호출기냉응액%고민C-반응단백%종류배사인자-α
Atorvastatin%Chronic obstructive pulmonary disease%Pulmonary arterial hypertension%Exhaled breath condensate%High sensitive C-reactive protein%Tumor necrosis factor-α
目的 分析慢性阻塞性肺疾病(COPD)继发的肺动脉高压(PAH)与炎症反应的相关性,研究阿托伐他汀对COPD合并PAH患者的治疗作用及可能机制.方法 收集我科稳定期单纯性COPD患者(40例),COPD合并PAH患者(45例)血清及呼出气冷凝液(EBC)标本,并常规行肺功能、动脉血气分析、超声心动图、6分钟步行距离(6MWD)、肝肾功能检测.乳胶增强透射免疫比浊法测定血清及EBC中高敏C-反应蛋白(hs-CRP).ELISA方法检测血清及EBC中肿瘤坏死因子-α(TNF-α).将稳定期COPD合并PAH患者随机分成治疗组(23例)和对照组(22例),对照组给予常规治疗,治疗组加用阿托伐他汀20 mg/d口服,6个月后观察两组的肺动脉压力、动脉血气分析、肺功能、6MWD、肝肾功能、血清及EBC中hs-CRP、TNF-α水平.结果 与单纯性COPD组相比,COPD合并PAH组PaO2、6MWD明显降低(P值均＜0.05),血清及EBC中hs-CRP、TNF-α水平明显增高(P值均＜0.05),且PaO2、6MWD与肺动脉收缩压(PASP)呈负相关(r=-0.472,P＜0.05;r=-0.435,P＜0.05),血清及EBC中hs-CRP、TNF-α均与PASP呈正相关(r=0.350～0.598,P值均＜0.05),6个月后,治疗组PASP力比同组治疗前和对照组治疗后均有明显降低(P＜0.05),差异有统计学意义；治疗组PaO2、6MWD比同组治疗前及对照组治疗后均有明显增高(P＜0.05),差异有统计学意义；两组血清及EBC中hs-CRP、TNF-α均明显降低(P值均＜0.05),但治疗组较对照组降低更明显,差异有统计学意义.结论全身及肺脏局部炎症反应可能参与了COPD继发的PAH形成过程.阿托伐他汀可降低COPD合并PAH患者肺动脉压力,改善动脉血氧分压及运动耐量,其机制可能与抑制全身及肺脏局部炎症反应有关.
目的 分析慢性阻塞性肺疾病(COPD)繼髮的肺動脈高壓(PAH)與炎癥反應的相關性,研究阿託伐他汀對COPD閤併PAH患者的治療作用及可能機製.方法 收集我科穩定期單純性COPD患者(40例),COPD閤併PAH患者(45例)血清及呼齣氣冷凝液(EBC)標本,併常規行肺功能、動脈血氣分析、超聲心動圖、6分鐘步行距離(6MWD)、肝腎功能檢測.乳膠增彊透射免疫比濁法測定血清及EBC中高敏C-反應蛋白(hs-CRP).ELISA方法檢測血清及EBC中腫瘤壞死因子-α(TNF-α).將穩定期COPD閤併PAH患者隨機分成治療組(23例)和對照組(22例),對照組給予常規治療,治療組加用阿託伐他汀20 mg/d口服,6箇月後觀察兩組的肺動脈壓力、動脈血氣分析、肺功能、6MWD、肝腎功能、血清及EBC中hs-CRP、TNF-α水平.結果 與單純性COPD組相比,COPD閤併PAH組PaO2、6MWD明顯降低(P值均＜0.05),血清及EBC中hs-CRP、TNF-α水平明顯增高(P值均＜0.05),且PaO2、6MWD與肺動脈收縮壓(PASP)呈負相關(r=-0.472,P＜0.05;r=-0.435,P＜0.05),血清及EBC中hs-CRP、TNF-α均與PASP呈正相關(r=0.350～0.598,P值均＜0.05),6箇月後,治療組PASP力比同組治療前和對照組治療後均有明顯降低(P＜0.05),差異有統計學意義；治療組PaO2、6MWD比同組治療前及對照組治療後均有明顯增高(P＜0.05),差異有統計學意義；兩組血清及EBC中hs-CRP、TNF-α均明顯降低(P值均＜0.05),但治療組較對照組降低更明顯,差異有統計學意義.結論全身及肺髒跼部炎癥反應可能參與瞭COPD繼髮的PAH形成過程.阿託伐他汀可降低COPD閤併PAH患者肺動脈壓力,改善動脈血氧分壓及運動耐量,其機製可能與抑製全身及肺髒跼部炎癥反應有關.
목적 분석만성조새성폐질병(COPD)계발적폐동맥고압(PAH)여염증반응적상관성,연구아탁벌타정대COPD합병PAH환자적치료작용급가능궤제.방법 수집아과은정기단순성COPD환자(40례),COPD합병PAH환자(45례)혈청급호출기냉응액(EBC)표본,병상규행폐공능、동맥혈기분석、초성심동도、6분종보행거리(6MWD)、간신공능검측.유효증강투사면역비탁법측정혈청급EBC중고민C-반응단백(hs-CRP).ELISA방법검측혈청급EBC중종류배사인자-α(TNF-α).장은정기COPD합병PAH환자수궤분성치료조(23례)화대조조(22례),대조조급여상규치료,치료조가용아탁벌타정20 mg/d구복,6개월후관찰량조적폐동맥압력、동맥혈기분석、폐공능、6MWD、간신공능、혈청급EBC중hs-CRP、TNF-α수평.결과 여단순성COPD조상비,COPD합병PAH조PaO2、6MWD명현강저(P치균＜0.05),혈청급EBC중hs-CRP、TNF-α수평명현증고(P치균＜0.05),차PaO2、6MWD여폐동맥수축압(PASP)정부상관(r=-0.472,P＜0.05;r=-0.435,P＜0.05),혈청급EBC중hs-CRP、TNF-α균여PASP정정상관(r=0.350～0.598,P치균＜0.05),6개월후,치료조PASP력비동조치료전화대조조치료후균유명현강저(P＜0.05),차이유통계학의의；치료조PaO2、6MWD비동조치료전급대조조치료후균유명현증고(P＜0.05),차이유통계학의의；량조혈청급EBC중hs-CRP、TNF-α균명현강저(P치균＜0.05),단치료조교대조조강저경명현,차이유통계학의의.결론전신급폐장국부염증반응가능삼여료COPD계발적PAH형성과정.아탁벌타정가강저COPD합병PAH환자폐동맥압력,개선동맥혈양분압급운동내량,기궤제가능여억제전신급폐장국부염증반응유관.
Objective The purpose of the present study was to investigate potential role of inflammation in pulmonary arterial hypertension (PAH)of chronic obstructive pulmonary disease (COPD),observe the effects of atorvastatin treatment in patients with COPD combining with PAH and explore the effect mechanism.Methods The forty patients with single COPD and forty-five stable COPD complicating PH participated in this study.Exhaled breath condensate (EBC) and serum of all cases were collected.Lung function,arterial blood gases,echocardiography,6-minute walking distance (6MWD),liver and kidney function were assayed in all cases.The levels of high sensitive C-reactive protein (hs-CRP) in serum and EBC were measured by latex enhanced transmission immunoturbidimetric assay.The level of tumor necrosis factor-α (TNF-α) in plasma and EBC were measured by a commercially available sandwich enzyme-linked immunoassay.Forty-five patients with stable COPD complicating PAH were randomly divided into treatment group (n =23) and control group (n =22).Two groups both received conventional therapy according to COPD.The former received atorvastatin 20 mg/d,and the latter without atorvastatin treatment.Pulmonary arterial pressure,arterial blood gas,pulmonary function,6MWD,liver and kidney function were detected and the blood samples and EBC collected before and 6 months after atorvastatin administration.Results The levels of arterial oxygen partial pressure (PaO2)and 6MWD in patients with pulmonary arterial hypertension were significially lower than that in patients without pulmonary arterial hypertension (P ＜0.05).The levels of hs-CRP and TNF-α in serum and EBC were significantly higher in patients with pulmonary arterial hypertension than in patients without pulmonary arterial hypertension (all P ＜0.05).Pulmonary artery systolic pressure (PASP) in PAH group was positively correlated with the levels of hs-CRP and TNF-α both in serum and EBC (r =0.350-0.598,all P ＜0.05).The PaO2 and 6MWD were correlated negatively with PASP (r =-0.472,P ＜0.05; r =-0.435,P ＜0.05).After 6 months of atorvastatin treatment,the PASP was significantly lower,the 6MWD and PaO2 were significantly higher in atorvastatin treatment group than in control group after 6 months treatment (P ＜0.05).The levels of hs-CRP and TNF-α both in serum and EBC were reduced obviously in the treatment group and control group,but the decline level in the treatment group was more obvious than that in the control group.Conclusions The inflammation reaction of system and local respiratory tracts may play an important role in the pathogenesis of pulmonary arterial hypertension of COPD.Atorvastatin can obviously reduce PASP,improve PaO2 and exercise tolerance of COPD patients combining with PAH.The mechanism may be that atorvastatin can inhibite the inflammatory reaction.
