Abstract
The first and clear indication that surface tension offers resistance to the initial lung aeration after birth came with von Neergaard’s study in 1929 [26]. He found that lungs that were collapsed would open up more readily if the effect of surface tension was completely nullified by using liquid rather than air as the expanding medium. Following this basic study, it took considerable time until Pattle in 1955 [19] could declare that he assumed there was an agent present in the lung that had the ability to depress surface tension to extremely low values. He extruded bubbles from the sectioned lung and found that when they were surrounded by saline, so that they could be studied under a microscope, they would quickly shrink 30% from their initial size, when their diameter was around 40 µ, but then the bubbles would persist for long periods of time (Fig. 1). Pattle reasoned that the high surface tension of water, 72 mN/m, ought to give an enormously high pressure in the tiny bubble, so that the gas inside the bubble should have been absorbed quickly by the surrounding saline solution. When this did not happen, but the bubble persisted, Pattle concluded that there must be a lining layer exerting surface pressure, almost completely counteracting the collapsing effect of water surface tension. The net surface tension according to Pattle must be very close to 0.
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© 1988 Springer-Verlag Berlin Heidelberg
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Enhorning, G. (1988). Pulmonary Surfactant: Evolution of Functional Concepts. In: Lachmann, B. (eds) Surfactant Replacement Therapy. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73305-5_1
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