Lipids, and phosphatidylcholines in particular, are major components in cell membranes and in human lung surfactant. Their ability to encapsulate or form stable layers suggests a significant role of the interfacial rheological properties. In the present work we focus on the surface rheological properties of dipalmitoylphosphatidylcholine (DPPC). Literature results are confusing and even contradictory; viscosity values have been reported differ by several orders of magnitude. Moreover, even both purely viscous and gel-like behaviours have been described. Assessing the literature critically, a limited experimental window has been explored correctly, which however does not yet include conditions relevant for the physiological state of DPPC in vivo. A complete temperature and surface pressure analysis of the interfacial shear rheology of DPPC is performed, showing that the monolayer behaves as a viscoelastic liquid with a domain structure. At low frequencies and for a thermally structured monolayer, the interaction of the molecules within the domains can be probed. The low frequency limit of the complex viscosity is measured over a wide range of temperatures and surface pressures. The effects of temperature and surface pressure on the low frequency viscosity can be analysed in terms of the effects of free molecular area. However, at higher frequencies or following a preshear at high shear rates, elasticity becomes important; most probably elasticity due to defects at the edge of the domains in the layer is probed. Preshearing refines the structure and induces more defects. As a result, disagreeing interfacial rheology results in various publications might be due to different pre-treatments of the interface. The obtained dataset and scaling laws enable us to describe the surface viscosity, and its dependence under physiological conditions of DPPC. The implications on functioning of lung surfactants and lung surfactant replacements will be discussed.

The surfactant lining the walls of the alveoli in the lungs increases pulmonary compliance and prevents collapse of the lung at the end of expiration. In premature born infants, surfactant deficiency causes problems, and lung surfactant replacements are instilled to facilitate breathing. These pulmonary surfactants, which form complex structured fluid-fluid interfaces, need to spread with great efficiency and once in the alveolus they have to form a thin stable film. In the present work, we investigate the mechanisms affecting the stability of surfactant-laden thin films during spreading, using drainage flows from a hemispherical dome. Three commercial lung surfactant replacements Survanta, Curosurf and Infasurf, along with the phospholipid dipalmitoylphosphatidylcholine (DPPC), are used. The surface of the dome can be covered with human alveolar epithelial cells and experiments are conducted at the physiological temperature. Drainage is slowed down due to the presence of all the different lung surfactant replacements and therefore the thin films show enhanced stability. However, a scaling analysis combined with visualization experiments demonstrates that different mechanisms are involved. For Curosurf and Infasurf, Marangoni stresses are essential to impart stability and interfacial shear rheology does not play a role, in agreement with what is observed for simple surfactants. Survanta, which was historically the first natural surfactant used, is rheologically active. For DPPC the dilatational properties play a role. Understanding these different modes of stabilization for natural surfactants can benefit the design of effective synthetic surfactant replacements for treating infant and adult respiratory disorders.

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