Pulmonary hypertension in chronic obstructive pulmonary disease: current theories of pathogenesis and their implications for treatment

被引:139
作者
Wright, JL
Levy, RD
Churg, A
机构
[1] Univ British Columbia, Dept Pathol, Vancouver, BC V6T 2B5, Canada
[2] Univ British Columbia, Dept Med, Vancouver, BC V6T 2B5, Canada
[3] St Pauls Hosp, Div Resp, Vancouver, BC V6Z 1Y6, Canada
关键词
D O I
10.1136/thx.2005.042994
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
The development of pulmonary hypertension is a poor prognostic sign in patients with chronic obstructive pulmonary disease ( COPD), affecting both mortality and quality of life. Although pulmonary hypertension in COPD is traditionally viewed as a result of emphysematous destruction of the vascular bed and/or hypoxia, recent studies indicate that neither of these factors correlates very well with pulmonary artery pressures. New human and animal experimental data are beginning to show that pulmonary hypertension in this setting is probably a result of the direct effect of tobacco smoke on the intrapulmonary vessels with abnormal production of mediators that control vasoconstriction, vasodilatation, and vascular cell proliferation, ultimately leading to aberrant vascular remodelling and aberrant vascular physiology. These changes are in many ways similar to those seen in other forms of pulmonary hypertension and suggest that the treatments used for primary pulmonary hypertension may be beneficial in patients with COPD.
引用
收藏
页码:605 / 609
页数:5
相关论文
共 40 条
[31]   Pulmonary vasoconstriction and hypertension in mice with targeted disruption of the endothelial nitric oxide synthase (NOS 3) gene [J].
Steudel, W ;
Ichinose, F ;
Huang, PL ;
Hurford, WE ;
Jones, RC ;
Bevan, JA ;
Fishman, MC ;
Zapol, WM .
CIRCULATION RESEARCH, 1997, 81 (01) :34-41
[32]   VASCULAR ENDOTHELIAL GROWTH-FACTOR INDUCES INTERSTITIAL COLLAGENASE EXPRESSION IN HUMAN ENDOTHELIAL-CELLS [J].
UNEMORI, EN ;
FERRARA, N ;
BAUER, EA ;
AMENTO, EP .
JOURNAL OF CELLULAR PHYSIOLOGY, 1992, 153 (03) :557-562
[33]   PROGNOSTIC VALUE OF PULMONARY-ARTERY PRESSURE IN CHRONIC OBSTRUCTIVE PULMONARY-DISEASE [J].
WEITZENBLUM, E ;
HIRTH, C ;
DUCOLONE, A ;
MIRHOM, R ;
RASAHOLINJANAHARY, J ;
EHRHART, M .
THORAX, 1981, 36 (10) :752-758
[34]  
WEITZENBLUM E, 1984, AM REV RESPIR DIS, V130, P993
[35]  
WRIGHT JL, 1983, AM REV RESPIR DIS, V128, P702
[36]   Cigarette smoke induces persisting increases of vasoactive mediators in pulmonary arteries [J].
Wright, JL ;
Tai, H ;
Churg, A .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2004, 31 (05) :501-509
[37]   A neutrophil elastase inhibitor reduces cigarette smoke-induced remodelling of lung vessels [J].
Wright, JL ;
Farmer, SG ;
Churg, A .
EUROPEAN RESPIRATORY JOURNAL, 2003, 22 (01) :77-81
[38]   Cigarette smoke induces rapid changes in gene expression in pulmonary arteries [J].
Wright, JL ;
Tai, H ;
Dai, J ;
Churg, A .
LABORATORY INVESTIGATION, 2002, 82 (10) :1391-1398
[39]   RELATIONSHIP OF PULMONARY ARTERIAL-PRESSURE AND AIR-FLOW OBSTRUCTION TO EMPHYSEMA [J].
WRIGHT, JL .
JOURNAL OF APPLIED PHYSIOLOGY, 1993, 74 (03) :1320-1324
[40]  
WRIGHT JL, 1992, LUNG, V170, P109