A microfluidic model of pumonary airway reopening in bifurcating networks
Acute Respiratory Distress Syndrome (ARDS) is a lung condition with a mortality rate of 40 % that affects about 225,000 individuals in the U.S. In these patients, epithelial injury can contribute to alveolar flooding and injury to type II cells by disrupting normal epithelial fluid transport, impacting the removal of edema fluid from alveolar space. Mechanical stresses associated with opening occluded airways damages the epithelial lining of the lungs. Prior studies explore the nature of the stresses and damage in straight tube models of airways. Our model presented in this work accounts for the branching in the pulmonary airways. We have developed a scalable microfluidic model of pulmonary airway bifurcations for investigation of reopening near the bifurcation as well as the macroscopic reopening pattern. We utilize a μ-PIV/Shadowgraph system to visualize the flow fields near the interface as a semi-infinite finger of air propagates through the bifurcation model. Further, we utilize μ-PIV for downstream flow-rate monitoring to examine the symmetry of reopening through bifurcating networks. In the absence of surfactant, propagation preferentially opens the low-resistance path, and leads to asymmetric reopening. However, with SDS and albumin inactivated surfactant, interfacial propagation preferentially reopens the pathway with the higher hydraulic resistance. The propagation pattern with pulmonary surfactant stabilizes the system so that the daughter branches of a nearly symmetric bifurcation open simultaneously. Our multiple generation network serves to validate the stability of the single generation. However, the second generation does not mirror the behavior of the first generation. We explore the reasons for this, and also present preliminary studies for the investigation of restoring surfactant function after deactivation by serum proteins.