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The **alveolar air-liquid interface surface tension** is the force exerted by water molecules lining the inner walls of alveoli, causing them to contract and potentially collapse[2][4][5]. In healthy lungs, **pulmonary surfactant**—secreted by type II alveolar cells—plays a critical role in reducing this surface tension, thereby stabilizing alveoli and facilitating efficient gas exchange[2][6]. Increased surface tension is a key factor in the pathogenesis of several lung diseases, such as ARDS and neonatal respiratory distress syndrome, where insufficient surfactant leads to alveolar collapse and impaired oxygen uptake[3][6]. While surfactant and its protein/phospholipid components serve as actual drug targets, the surface tension itself is a biophysical phenomenon targeted indirectly through surfactant therapy[3][6].
Lowering alveolar surface tension by providing or restoring normal surfactant activity
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