Mechanisms underlying the surface properties of lung surfactant are extensively studied in in vitro systems such as the captive-bubble surfactometer (CBS), the pulsating-bubble surfactometer, and the Wilhelmy balance. Among these systems, the CBS is advantageous when a leakproof system and high cycling rates are required. However, widespread application of the CBS to mechanistic studies of dynamic surfactant protein-phospholipid interactions of spread film and to comparative studies between spread and adsorbed film is hampered because spreading of film is difficult. In addition, when film is formed by adsorption, the amount of material required is fairly large. We have developed an easy spreading technique that allows routine formation of film by spreading of small amounts of surfactant components at the air-water interface of an air bubble in a CBS. The technique is reliable, precise, and accurate, and the biophysical activity of film formed by spreading is similar to that of film formed by adsorption. This method will be useful for mechanistic studies of surfactant components under dynamic conditions and for comparative studies of spread films and adsorbed films.

The biophysical activity of lung surfactant depends, to a large extent, on the presence of the hydrophobic surfactant proteins B (SP-B) and C (SP-C). The role of these proteins in lipid adsorption and lipid squeeze-out under dynamic conditions simulating breathing is not yet clear. Therefore, the aim of this study was to investigate the interaction of spread hydrophobic surfactant proteins with phospholipids in a captive-bubble surfactometer during rapid cyclic area changes (6 cycles/min). We found that SP-B and SP-C facilitated the rapid transport of lipids into the air-water interface in a concentration-dependent manner (threshold concentration > or = 0.05:0.5 mol% SP-B/SP-C). Successive rapid cyclic area changes did not affect the concentration-dependent lipid adsorption process, suggesting that SP-B and SP-C remained associated with the surface film.

When conventional mechanical ventilation was used in lipopolysaccharide-induced lung injury, surfactant preferentially distributed into underinflated and aerated alveolar areas. Because surfactant rarely reached collapsed alveolar areas, methods aiding in alveolar recruitment (e.g., open lung concept or body positioning) should precede surfactant administration.

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