Pride N B, Ingram R H, Lim T K
Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
Am Rev Respir Dis. 1991 Jun;143(6):1446-9. doi: 10.1164/ajrccm/143.6.1446.
The extent of air-space destruction caused by emphysema is very variable in severe chronic obstructive pulmonary disease (COPD), constituting one of the most obvious differences between COPD and asthma. Differences in the static deflation pressure-volume curve between COPD and asthma can easily be shown, but it has been surprisingly difficult to find distinctive mechanical features of impaired airway function caused by air-space destruction. This may be because in mild airway obstruction related to smoking--particularly in younger subjects--emphysema may be absent, and the predominant site of airway narrowing in the smallest bronchi and respiratory bronchioles may be the same as that found in asthma in remission. In more severe obstruction caused by COPD there is almost always very severe intrinsic disease of the airways and this may so dominate the functional abnormality that it is difficult to detect any additional change because of airspace destruction. Overall, few studies have set out to detect specific effects of parenchymal destruction on airway function.
在重度慢性阻塞性肺疾病（COPD）中，肺气肿所致的气腔破坏程度差异很大，这是COPD与哮喘之间最明显的区别之一。COPD和哮喘之间的静态呼气压力-容积曲线差异很容易显示出来，但令人惊讶的是，很难找到气腔破坏导致气道功能受损的独特力学特征。这可能是因为在与吸烟相关的轻度气道阻塞中——尤其是在较年轻的受试者中——可能不存在肺气肿，最小支气管和呼吸性细支气管气道狭窄的主要部位可能与哮喘缓解期相同。在COPD导致的更严重阻塞中，气道几乎总是存在非常严重的内在疾病，这可能在功能异常中占主导地位，以至于由于气腔破坏而难以检测到任何额外变化。总体而言，很少有研究专门去检测实质破坏对气道功能的具体影响。
