Abstract

Pulmonary surfactant (PS), a lipo-protein complex, regulates interfacial surface tension of the lung. The fluctuations in body temperatures of heterothermic mammals correlate with fluctuations in surfactant lipid composition as well as function. Previously we speculated that the higher levels of cholesterol during torpor will reduce phase transition temperature (Tm) enabling PS to remain fluid over a broader range of temperatures. However, these compositional changes do not explain how the surfactant can attain low surface tensions without suffering film collapse at the interface.

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