Luminal epithelial projections formed during bronchoconstriction define interstices in which liquid can collect. Liquid in these interstices could amplify the degree of luminal compromise due to muscular contraction in at least two distinct ways. First, the luminal cross-sectional area is reduced by simple filling of the interstices. Second, if the surface tension (gamma) of the air-liquid interface is positive, the pressure drop across the interface produces an additional inward force that can further constrict the airway. We present a theoretical treatment of these two mechanisms together with data which suggest that both may significantly amplify the luminal narrowing due to airway smooth muscle contraction, particularly in small airways when gamma is high. To qualitatively assess the effects of altered gamma, guinea pig lungs with normal and altered airway liquid lining layers were frozen and studied while fully hydrated by low-temperature scanning electron microscopy. Airway gamma was altered in these animals by intratracheal instillation of 0.5 mg lysoplatelet-activating factor (lyso-PAF). The interstices of normal airways were dry, whereas the interstices of airways with altered surface lining layers were liquid filled. In addition, the surfactant inhibitory properties of lyso-PAF, 2-arachidonyl-PAF, and dipalmitoyl phosphatidylcholine (DPPC) were measured with a pulsating bubble surfactometer, using surfactant TA as the model surfactant. Minimal gamma (gamma min) of surfactant TA alone was 4.0 +/- 0.2 dyn/cm; a 5% mixture of lyso-PAF with surfactant TA resulted in a significantly (P less than 0.02) greater gamma min of 8.8 +/- 1.8 dyn/cm. In contrast, 2-arachidonyl-PAF and DPPC had minimal effects on gamma min of surfactant TA.