On the mechanism of mucosal folding in normal and asthmatic airways

Barry R. Wiggs 1 , Constantine A. Hrousis 1 , Jeffrey M. Drazen 2 , and Roger D. Kamm 1 1 Center for Biomedical Engineering and the Department of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge, 02139; and 2 Division of Respiratory and Critical Care Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115 Received 30 July 1996; accepted in final form 1 August 1997. Wiggs, Barry R., Constantine A. Hrousis, Jeffrey M. Drazen, and Roger D. Kamm. On the mechanism of mucosal folding in normal and asthmatic airways. J. Appl. Physiol. 83(6): 1814-1821, 1997. 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. asthma; epithelium; mechanics; finite-element analysis; remodeling; computational model 0161-7567/97 $5.00 Copyright © 1997 the American Physiological Society