Sturm R, Hofmann W
Division of Physics and Biophysics, Department of Molecular Biology, University of Salzburg, Salzburg, Austria.
J Aerosol Med. 2004 Winter;17(4):357-72. doi: 10.1089/jam.2004.17.357.
In the present study, disease-specific stochastic models were developed for the computation of particle deposition in lungs affected by COPD, emphysema, or both, distinguishing between four types of pulmonary emphysema-centriacinar, paraseptal, panacinar, and bullous. To simulate COPD, airway calibers of the tracheobronchial tree were randomly reduced between 20% and 50% in each airway. For the study of pure COPD ("blue bloaters"), alveolated airway dimensions of the healthy lung were used, while for the simulation of emphysema without COPD ("pink puffers"), normal conductive airway diameters were assumed. Deposition calculations in diseased lungs were carried out by assuming (a) identical inspiration and expiration times (no breath-hold time) and (b) a continuous increase of the functional residual capacity (from 3,300 to 5,000 mL), accompanied by a simultaneous drop of the tidal volume (from 1,000 to 500 mL). Independent of particle size, total alveolar deposition in emphysematous lungs was significantly decreased relative to normal lungs. In particular, the deposition maximum at large particle sizes, which is a characteristic for healthy subjects, completely disappeared. Among the various emphysema models, deposition was smallest in lungs with bullous emphysema due to strongly enhanced settling and diffusion distances within the alveolar structures. A change of the lung volume caused a further decrease in particle deposition. Alveolar deposition in "blue bloaters" and "pink puffers" was very similar to the deposition in patients suffering from COPD and emphysema. Alveolar deposition per acinar airway generation was also strongly reduced in diseased lungs compared to normal lungs. Besides this reduction, deposition patterns became more uniform throughout the alveolar region.
在本研究中,开发了疾病特异性随机模型,用于计算慢性阻塞性肺疾病(COPD)、肺气肿或两者兼有的肺部颗粒沉积情况,区分了四种类型的肺气肿——小叶中心型、间隔旁型、全小叶型和大疱型。为了模拟COPD,气管支气管树的气道管径在每个气道中随机缩小20%至50%。对于单纯COPD(“蓝肿型”)的研究,使用健康肺的肺泡气道尺寸,而对于无COPD的肺气肿(“粉喘型”)模拟,假设传导气道直径正常。通过假设(a)吸气和呼气时间相同(无屏气时间)以及(b)功能残气量持续增加(从3300毫升增加到5000毫升),同时潮气量下降(从1000毫升下降到500毫升),来进行患病肺部的沉积计算。与正常肺相比,无论颗粒大小如何,肺气肿肺部的总肺泡沉积均显著减少。特别是,健康受试者特有的大颗粒尺寸下的沉积最大值完全消失。在各种肺气肿模型中,由于肺泡结构内沉降和扩散距离显著增加,大疱性肺气肿肺部的沉积最小。肺容积的变化导致颗粒沉积进一步减少。“蓝肿型”和“粉喘型”的肺泡沉积与COPD和肺气肿患者的沉积非常相似。与正常肺相比,患病肺中每个腺泡气道级别的肺泡沉积也显著减少。除了这种减少外,整个肺泡区域的沉积模式变得更加均匀。