Abstract
Pulmonary surfactant (PS) is a lipid-protein mixture lining the alveolar air-water interface. By lowering surface tension, PS stabilizes the respiratory surface, thereby impeding alveolar collapse. Lack or alterations of PS properties are associated with acute lung injury (ALI). Sevoflurane is widely used in medical practice; however, some adverse properties were described in the lung function and PS [1,2]. The hypothesis of this study is that Sevoflurane affects native PS (NPS) system, which may contribute to ALI during anesthesia. In the present work, we have analyzed the functional, structural, and thermodynamic properties of NPS and its membranes reconstituted from the organic lipid extract (EPS) upon exposure to Sevoflurane. The compression-expansion properties of NPS films exposed to Sevoflurane were analyzed in a captive bubble surfactometer (CBS) as well as the effects of the anesthetic on the thermotropic properties of NPS and EPS membranes.Q-Static and dynamic cycles of NPS films were strongly affected upon exposure to Sevoflurane, which diminished the ability of the films to reach very low surface tension during compression. However, the equilibrium surface tension after adsorption and the maximum surface tension at the end of the expansion moieties of cycling isotherms were not affected by the presence of Sevoflurane. Spectroscopic analysis of surfactant complexes doped with LAURDAN or diphenylhexatriene indicate fluidification of EPS membranes upon exposure to Sevoflurane at room temperature. DSC experiments indicated that Sevoflurane induces a decrease of Tm and ΔH associated with the main thermotropic transition in PS membranes.In conclusion, the present results indicate that Sevoflurane impairs the biophysical properties of PS through perturbation of the lateral order of segregated phases, compromising correct compression along the respiratory cycles.[1] L. Malacrida et al. Am. J. Respir. Crit. Care Med.181;2010:A3631.[2] L. Malacrida et al. Biophysical J. 100(3);2011:505a-506a.
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