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Micro-PIV Measurements of an Airway Closure Model

[+] Author Affiliations
Shiyao Bian, Ying Zheng, Shuichi Takayama, James B. Grotberg

University of Michigan, Ann Arbor, MI

Paper No. SBC2009-206831, pp. 141-142; 2 pages
  • ASME 2009 Summer Bioengineering Conference
  • ASME 2009 Summer Bioengineering Conference, Parts A and B
  • Lake Tahoe, California, USA, June 17–21, 2009
  • Conference Sponsors: Bioengineering Division
  • ISBN: 978-0-7918-4891-3
  • Copyright © 2009 by ASME


A thin liquid layer coating the airway can be unstable and forms a plug. Airway closure usually happens at the small airways near the end of expiration, often accompanied with hypersecretion or/and surfactant deficiency in the airway in a variety of lung diseases, such as chronic obstructive pulmonary disease (COPD) and acute respiratory distress syndrome (ARDS). Modeling work by Halpern and Grotberg [1] has shown that several forces could contribute to airway closure, such as the surface tension instability and the wall compliance. Experiments in a capillary tube were conducted by Cassidy et al. [2] who found that adding surfactant increased the airway closure time and the critical film thickness. In vitro studies [3] [4] illustrated that exposure of primary human airway epithelial cells to plug propagation and rupture led to significant cell injury. Experimental studies [5] [6] on excised lungs or in vivo animal models have shown that severe tissue damage was found in surfactant-deficient lungs due to the repetitive airway reopening. However, mechanical forces induced by airway closure have not been experimentally evaluated.

Copyright © 2009 by ASME



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