Wiggs B R, Hrousis C A, Drazen J M, Kamm R D
Center for Biomedical Engineering and the Department of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge, 02139, Boston, Massachusetts 02115, USA.
J Appl Physiol (1985). 1997 Dec;83(6):1814-21. doi: 10.1152/jappl.1997.83.6.1814.
Previous studies have demonstrated that the airway wall in asthma and chronic obstructive pulmonary disease is markedly thickened. It has also been observed that when the smooth muscle constricts the mucosa buckles, forming folds that penetrate into the airway lumen. This folding pattern may influence the amount of luminal obstruction associated with smooth muscle activation. A finite-element analysis of a two-layer composite model for an airway is used to investigate the factors that determine the mucosal folding pattern and how it is altered as a result of changes in the thickness or stiffness of the different layers that comprise the airway wall. Results demonstrate that the most critical physical characteristic is the thickness of the thin inner layer of the model. Thickening of this inner layer likely is represented by the enhanced subepithelial collagen deposition seen in asthma. Other findings show a high shear stress at or near the epithelial layer, which may explain the pronounced epithelial sloughing that occurs in asthma, and steep gradients in pressure that could cause significant shifts of liquid between wall compartments or between the wall and luminal or vascular spaces.
先前的研究表明，哮喘和慢性阻塞性肺疾病患者的气道壁明显增厚。还观察到，当平滑肌收缩时，黏膜会发生褶皱，形成深入气道管腔的皱襞。这种褶皱模式可能会影响与平滑肌激活相关的管腔阻塞程度。利用气道双层复合模型的有限元分析来研究决定黏膜褶皱模式的因素，以及由于构成气道壁的不同层的厚度或刚度变化而导致的褶皱模式改变。结果表明，最关键的物理特性是模型薄内层的厚度。该内层增厚可能表现为哮喘中所见的上皮下胶原沉积增加。其他研究结果显示，上皮层或其附近存在高剪切应力，这可能解释了哮喘中发生的明显上皮脱落，以及压力的陡峭梯度，这可能导致壁腔之间或壁与管腔或血管空间之间的液体显著转移。
