Objective To explore the ultrastructure characteristics of pulmonary arteries in smokers with normal lung function and with chronic obstructive pulmonary disease ( COPD) . Methods 33 patients who undertook surgery for peripheral lung cancer were collected. According to smoking history and pulmonary function, the patients were divided into three groups, ie. non-smokers with normal pulmonary function ( group A, n = 10) , smokers with normal pulmonary function ( group B, n = 13) , and smokers in stable phase of COPD ( group C, n = 10) . Normal lung tissues without cancer were sampled and observed under light and electric microscope. Results ①Compared with group A, the thickness of intimal layer of intra-acinar pulmonary muscular arteries of group B and C were significantly higher, the area of their lumen
was lower, and the proportion of their muscular arteries was higher( P lt; 0. 01) . ②Ultrastructure of small pulmonary arteries of group A showed that intimal layer was normal, so as to endothelial cells and smooth muscle cells. Collagen fiber was not increased. Ultrastructure observation of group B showed that endothelial
cells were distorted, basal membrane was thick, and collagen fiber increased in vessels. Ultrastructure observation of group C showed that endothelial cells degenerated, vascular intima thickness increased, andsynthetic phenotype smooth muscle cells increased. ③ Smoking index was positively correlated with the
proportion of muscular arteries and the proportion of intimal area( r =0. 464,0. 635, P lt;0. 05, respectively) ,and negatively correlated with the proportion of lumen area( r= - 0. 603, P lt;0. 05) . Conclusions Smokers with normal lung fuction and with COPD show the similar ultrastructural characterizations in endothelial cells, smooth muscle cells, and pulmonary arterial remodeling, which related closely to smoking.
Citation：
ZHANG Jianquan,CHEN Xunxun,LIANG Yi,LIANG Ying,ZHONG Xiaoning.. Ultrastructure of Pulmonary Small Arteries in Smokers with Normal Lung Function and with Chronic Obstructive Pulmonary Disease. Chinese Journal of Respiratory and Critical Care Medicine, 2010, 9(5): 465-470. doi:
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Copyright © the editorial department of Chinese Journal of Respiratory and Critical Care Medicine of West China Medical Publisher. All rights reserved
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Peinado VI, Pizarro S, Barbera JA. Pulmonary vascular involvement in COPD. Chest, 2008 , 134: 808-814.
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张建全, 钟小宁, 刘积锋, 等. 血管内皮生长因子与慢性支气管炎并肺气肿大鼠早期肺动脉重塑关系的研究. 国际呼吸杂志,2007, 27: 166-170 .
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- 1. Zhong N, Wang C, Yao W, et al. Prevalence of chronic obstructive pulmonary disease in China: a large, population-based survey. Am J Respir Crit Care Med, 2007, 176: 753-760 .
- 2. Global Initiative for Chronic Obstructive Lung Disease ( GOLD) .Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease NHLBI/WHO workshop report. Rev. ed. 2007. ( Accessed December 28, 2007).
- 3. Geijer RM, Sachs AP, Verheij TJ, et al. Incidence and determinants of moderate COPD ( GOLD II) in male smokers aged 40-65 years:5 -year follow up. Br J Gen Pract, 2006, 56: 656-661.
- 4. BarberàJA, Peinado VI, Santos S. Pulmonary hypertension in chronic obstructive pulmonary disease. Eur Respir J, 2003, 21: 892-905.
- 5. Wright JL, Levy RD, Churg A. Pulmonary hypertension in chronic obstructive pulmonary disease: current theories of pathogenesis and their implications for treatment. Thorax, 2005, 60: 605 -609.
- 6. 张建全, 钟小宁, 蒋明, 等. 慢性支气管炎、肺气肿时肺动脉高压与肺动脉壁改建与炎症的关系. 中国病理生理杂志, 2006, 22 :1811-1815.
- 7. Battaglia S, Mauad T, van Schadewijk AM, et al. Differential distribution of inflammatory cells in large and small airways in smokers. J Clini Patho, 2007, 60: 907-911 .
- 8. Peinado VI, Pizarro S, Barbera JA. Pulmonary vascular involvement in COPD. Chest, 2008 , 134: 808-814.
- 9. 刘积锋, 钟小宁, 何志义, 等. 慢性支气管炎合并肺气肿大鼠非低氧血症期肺动脉重塑的特点及N-乙酰半胱氨酸的作用. 中华结核和呼吸杂志, 2007, 30: 713 -715.
- 10. 张建全, 钟小宁, 刘积锋, 等. 血管内皮生长因子与慢性支气管炎并肺气肿大鼠早期肺动脉重塑关系的研究. 国际呼吸杂志,2007, 27: 166-170 .
