Acute respiratory distress syndrome (ARDS) is a severe lung disease caused by a variety of direct and indirect insults. During ARDS edema fluid accumulated in the lung inhibits gas exchange between air and blood. The main treatment for ARDS is mechanical ventilation. The ventilation of fluid filled lungs involves the propagation of microbubbles over a layer of epithelial cells as shown in Figure 1. Unfortunately, experimental studies[1,3] have demonstrated that the large shear and normal stress gradients generated by microbubbles cause significant cellular deformation and injury. As a result, the mortality rates for ARDS is high (～30-40%). Previous investigators have numerically modeled the fluid mechanical aspects[1,2] or the cellular deformation aspects[5] of airway reopening. However, these models do not account for the complex fluid-structure interactions that occur both in-vitro and invivo. Specifically, deformation of the air-liquid interface may influence cellular deformation and vice-versa. In addition, pulmonary airways are compliant and changes in airway wall mechanics may significantly influence the dynamics of airway reopening [4] and cellular deformation.
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