In this study, our goal is to identify the interaction between airway lining fluid viscous and surface forces and parenchymal tethering forces during pulmonary airway reopening. The type of closure we modeled occurs when the airway walls and surrounding parenchyma collapse and are held in apposition by the lining fluid. We mimicked this system with a polyethylene tube coated with a Newtonian lining fluid supported by open-cell foam. Reopening occurs when a finger of air travels through the collapsed region. We measured the airway pressure (Paw) required to open the airway at a constant velocity (U). Increasing the foam stiffness (K), lining fluid viscosity (mu), and surface tension (gamma) results in an increase in Paw. Furthermore, increasing the downstream suction pressure (Pds), through tethering, causes an equivalent reduction in Paw. The upstream radius is the primary length scale, and fluid forces are represented by the capillary number: Ca = microU/gamma. On the basis of these results, we predicted the likelihood that tethering would begin to reopen collapsed airways in various disease states. This analysis showed that the ratio of tethering to fluid forces determines airway patency, which is defined as follows: lambda = PTrans/(gamma/R), where PTrans = Paw-Pds and R is airway radius. Finally, lung volume-dependent surface tension appears to be necessary to stabilize the lung.