慢性阻塞性肺疾病相关肺动脉高压发病机制

doi:10.3969/j.issn.1004-583X.2016.03.029

摘要/Abstract

摘要： 慢性阻塞性肺疾病(COPD)是危害人类健康的常见病、多发病,近年来发病率及病死率不断上升。肺动脉高压(PH)是一种血流动力学及病理生理学异常状态,见于多种疾病。COPD患者因吸烟、慢性缺氧、炎症反应等因素,通过反应活性氧类(ROS)、炎症因子、细胞因子、离子通道多个途径共同作用,引起肺血管收缩、原位微血栓形成、血液黏稠度增加、肺血管重塑,同时由于肺部病变导致毛细血管丢失,使肺血管阻力(PVR)升高,促进COPD相关性PH的形成与发展,右心后负荷增加,长期作用可导致慢性肺源性心脏病,严重增加疾病负担,影响患者生活质量及预后。目前COPD相关性PH主要治疗措施为氧疗,尚无确切有效药物。

关键词: 肺疾病, 慢性阻塞性, 高血压, 肺性, 缺氧, 炎症反应

中图分类号:

R563.9

贾佳,程德云. 慢性阻塞性肺疾病相关肺动脉高压发病机制[J]. 临床荟萃, 2016, 31(3): 345-348.

导出引用管理器 EndNote|Ris|BibTeX

链接本文: https://huicui.hebmu.edu.cn/CN/10.3969/j.issn.1004-583X.2016.03.029

https://huicui.hebmu.edu.cn/CN/Y2016/V31/I3/345

参考文献

[1] Oswald-Mammosser M, Weitzenblum E, Quoix E, et al. Prognostic factors in COPD patients receiving long-term oxygen therapy. Importance of pulmonary artery pressure[J]. Chest, 1995, 107(5): 1193-1198.
[2] Kessler R, Faller M, Fourgaut G, et al. Predictive factors of hospitalization for acute exacerbation in a series of 64 patients with chronic obstructive pulmonary disease[J]. Am J Respir Crit Care Med, 1999, 159(1): 158-164.
[3] Idrees MM, Saleemi S, Azem MA, et al. Saudi guidelines on the diagnosis and treatment of pulmonary hypertension: 2014 updates[J]. Ann Thorac Med, 2014, 9(Suppl 1):S1-S15.
[4] Minai OA, Chaouat A, Adnot S. Pulmonary hypertension in COPD: epidemiology, significance, and management: pulmonary vascular disease: the global perspective[J]. Chest, 2010, 137(6 Suppl):39S-51S.
[5] Chaouat A, Naeije R, Weitzenblum E. Pulmonary hypertension in COPD[J]. Eur Respir J, 2008,32(5): 1371-1385.
[6] Hyduk A, Croft JB, Ayala C, et al. Pulmonary hypertension surveillance--United States, 1980-2002[J]. MMWR Surveill Summ, 2005, 54(5): 1-28.
[7] Thabut G, Dauriat G, Stern JB, et al. Pulmonary hemodynamics in advanced COPD candidates for lung volume reduction surgery or lung transplantation[J]. Chest, 2005, 127(5): 1531-1536.
[8] Chaouat A, Bugnet AS, Kadaoui N, et al. Severe pulmonary hypertension and chronic obstructive pulmonary disease[J]. Am J Respir Crit Care Med, 2005, 172(2): 189-194.
[9] Yoshida T, Tuder RM. Pathobiology of cigarette smoke-induced chronic obstructive pulmonary disease[J]. Physiol Rev, 2007, 87(3):1047-1082.
[10] Wright JL, Tai H, Churg A. Vasoactive mediators and pulmonary hypertension after cigarette smoke exposure in the guinea pig[J]. J Appl Physiol (1985), 2006, 100(2): 672-678.
[11] Zhao L, Wang J, Wang L, et al. Remodeling of rat pulmonary artery induced by chronic smoking exposure[J]. J Thorac Dis, 2014, 6(6): 818-828.
[12] Santos S, Peinado VI, Ramírez J, et al. Characterization of pulmonary vascular remodelling in smokers and patients with mild COPD[J]. Eur Respir J, 2002, 19(4): 632-638.
[13] Hale KA, Ewing SL, Gosnell BA, et al. Lung disease in long-term cigarette smokers with and without chronic air-flow obstruction[J]. Am Rev Respir Dis, 1984, 130(5): 716-721.
[14] Peinado VI, Barberá JA, Abate P, et al. Inflammatory reaction in pulmonary muscular arteries of patients with mild chronic obstructive pulmonary disease[J]. Am J Respir Crit Care Med, 1999, 159(5 Pt 1):1605-1611.
[15] 张建全,钟小宁,蒋明,等. 慢支、肺气肿并肺动脉高压的特征及其机制探讨[J]. 广西医科大学学报, 2006,23(3): 375-378.
[16] Li J, Li JJ, He JG, et al. Atorvastatin decreases C-reactive protein-induced inflammatory response in pulmonary artery smooth muscle cells by inhibiting nuclear factor-κB pathway[J]. Cardiovasc Ther, 2010, 28(1): 8-14.
[17] Joppa P, Petrasova D, Stancak B, et al. Systemic inflammation in patients with COPD and pulmonary hypertension[J]. Chest, 2006, 130(2): 326-333.
[18] Eddahibi S, Chaouat A, Tu L, et al. Interleukin-6 gene polymorphism confers susceptibility to pulmonary hypertension in chronic obstructive pulmonary disease[J]. Proc Am Thorac Soc, 2006, 3(6): 475-476.
[19] Quarck R, Nawrot T, Meyns B, et al. C-reactive protein new predictor of adverse outcome in pulmonary arterial hypertension[J]. J Am Coll Cardiol, 2009, 53(14): 1211-1218.
[20] Stenmark KR, Fagan KA, Frid MG. Hypoxia-induced pulmonary vascular remodeling: cellular and molecular mechanisms[J]. Circ Res, 2006, 99(7): 675-691.
[21] Fishman AP. Hypoxia on the pulmonary circulation. How and where it acts[J]. Circ Res, 1976, 38(4): 221-231.
[22] Archer S, Michelakis E. The mechanism(s) of hypoxic pulmonary vasoconstriction potassium channels, redox O(2) sensors, and controversies[J]. News Physiol Sci, 2002,17: 131-137.
[23] 周荣,刘良明. 血管平滑肌肌浆网膜RyR2调节血管反应性的研究进展[J].生理科学进展, 2012,43(1):41-44.
[24] 胡颖,格日力. 离子通道在肺动脉的分布及在低氧肺血管收缩反应中的作用[J].生理科学进展, 2006,37(2): 113-116.
[25] Albarwani S, Heinert G, Turner JL, et al. Differential K⁺ channel distribution in smooth muscle cells isolated from the pulmonary arterial tree of the rat[J]. Biochem Biophys Res Commun, 1995, 208(1):183-189.
[26] 杨张娅,刘斌. ROCK信号通路在血管平滑肌细胞增殖和迁移作用中的研究进展[J].实用心脑肺血管病杂志, 2013, 21(3):10-12.
[27] Jin HG, Yamashita H, Nagano Y, et al. Hypoxia-induced upregulation of endothelial small G protein RhoA and Rho-kinase/ROCK2 inhibits eNOS expression[J]. Neurosci Lett, 2006, 408(1): 62-67.
[28] 王辰,杜敏捷,曹大德,等.慢性肺原性心脏病急性发作期肺细小动脉血栓形成的病理观察[J]. 中华医学杂志, 1997,77(2): 44-46+82.
[29] Timms RM, Khaja FU, Williams GW. Hemodynamic response to oxygen therapy in chronic obstructive pulmonary disease[J]. Ann Intern Med, 1985, 102(1): 29-36.
[30] Magee F, Wright JL, Wiggs BR, et al. Pulmonary vascular structure and function in chronic obstructive pulmonary disease[J]. Thorax, 1988, 43(3): 183-189.
[31] Wilkinson M, Langhorne CA, Heath D, et al. A pathophysiological study of 10 cases of hypoxic cor pulmonale[J]. Q J Med, 1988, 66(249): 65-85.
[32] Wang PP, Kong FP, Chen XQ, et al. HIF- 1 signal pathway in cellular response to hypoxia[J]. J Zhejiang Univ ( Medical Sci), 2011,40(5): 559- 566.
[33] Faller DV. Endothelial cell responses to hypoxic stress[J]. Clin Exp Pharmacol Physiol, 1999, 26(1): 74-84.
[34] 袁雅冬,宫小薇.2014年呼吸系统疾病临床进展[J].临床荟萃,2015,30(2):135-141.