University of British Columbia James Hogg Research Centre, St. Paul's Hospital, Vancouver, BC, Canada.
N Engl J Med. 2011 Oct 27;365(17):1567-75. doi: 10.1056/NEJMoa1106955.
The major sites of obstruction in chronic obstructive pulmonary disease (COPD) are small airways (<2 mm in diameter). We wanted to determine whether there was a relationship between small-airway obstruction and emphysematous destruction in COPD.
We used multidetector computed tomography (CT) to compare the number of airways measuring 2.0 to 2.5 mm in 78 patients who had various stages of COPD, as judged by scoring on the Global Initiative for Chronic Obstructive Lung Disease (GOLD) scale, in isolated lungs removed from patients with COPD who underwent lung transplantation, and in donor (control) lungs. MicroCT was used to measure the extent of emphysema (mean linear intercept), the number of terminal bronchioles per milliliter of lung volume, and the minimum diameters and cross-sectional areas of terminal bronchioles.
On multidetector CT, in samples from patients with COPD, as compared with control samples, the number of airways measuring 2.0 to 2.5 mm in diameter was reduced in patients with GOLD stage 1 disease (P=0.001), GOLD stage 2 disease (P=0.02), and GOLD stage 3 or 4 disease (P<0.001). MicroCT of isolated samples of lungs removed from patients with GOLD stage 4 disease showed a reduction of 81 to 99.7% in the total cross-sectional area of terminal bronchioles and a reduction of 72 to 89% in the number of terminal bronchioles (P<0.001). A comparison of the number of terminal bronchioles and dimensions at different levels of emphysematous destruction (i.e., an increasing value for the mean linear intercept) showed that the narrowing and loss of terminal bronchioles preceded emphysematous destruction in COPD (P<0.001).
These results show that narrowing and disappearance of small conducting airways before the onset of emphysematous destruction can explain the increased peripheral airway resistance reported in COPD. (Funded by the National Heart, Lung, and Blood Institute and others.).
慢性阻塞性肺疾病（COPD）的主要阻塞部位是小气道（直径<2 毫米）。我们想要确定小气道阻塞与 COPD 中气肿性破坏之间是否存在关系。
我们使用多排螺旋 CT（CT）比较了 78 例因全球慢性阻塞性肺疾病倡议（GOLD）评分而处于不同 COPD 阶段的患者的孤立肺和肺移植患者的孤立肺中的直径为 2.0 至 2.5 毫米的气道数量，以及供体（对照）肺。使用微 CT 测量肺气肿程度（平均线性截距）、每毫升肺容积的终末细支气管数量以及终末细支气管的最小直径和横截面积。
在多排螺旋 CT 上，与对照样本相比，GOLD 1 期疾病患者（P=0.001）、GOLD 2 期疾病患者（P=0.02）和 GOLD 3 或 4 期疾病患者（P<0.001）的直径为 2.0 至 2.5 毫米的气道数量减少。GOLD 4 期疾病患者的孤立肺样本的微 CT 显示，终末细支气管的总横截面积减少了 81%至 99.7%，终末细支气管的数量减少了 72%至 89%（P<0.001）。比较不同程度气肿性破坏下的终末细支气管数量和尺寸（即平均线性截距的增加值）表明，COPD 中的终末细支气管变窄和消失先于气肿性破坏（P<0.001）。
这些结果表明，在气肿性破坏发生之前，小传导气道的变窄和消失可以解释 COPD 中报告的外周气道阻力增加。（由美国国立心肺血液研究所等资助）。
