Acute respiratory distress syndrome (ARDS) and infant respiratory distress syndrome (IRDS) are severe pulmonary syndromes affecting approximately 190,000 in the United States with a mortality rate of 40%. During ARDS, hypoxemia can follow, which requires mechanical ventilation. This assisted ventilation can injure the lung by inducing large mechanical stresses from an air-liquid interface propagating through occlusion, and exposing the vessel wall to large mechanical stress gradients. In this study we investigate airway reopening scenarios by creating a model of terminal pulmonary airways using flexible tubing with monolayer coverage of lung epithelial cells. Specifically, we attempt to find a relationship between the state of collapse of a channel and the stress the cells undergo during the reopening event. This study is the first demonstration of an experimental tube with a tube law approximately physiological range. Our results indicated that in collapsed channels, as the velocity of reopening increases, the amount of damage to cells increases. This indicates flexibility causes an increase in cell damage which agrees with the stimulus-response behavior from prior studies. However, in fully-inflated channels, we see transitional behavior between flexible and rigid models. This research is a good starting point to investigate recruitment-derecruitment events in flexible channels, which could give a better representation of the mechanisms that cause cell damage in cases of ARDS and VILI. / 1 / Michael C Harrison