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Inhibition of Pulmonary Surfactant Adsorption by Serum and the Mechanisms of Reversal by Hydrophilic Polymers: Theory

Joseph A. Zasadzinski ^*, T. F. Alig ^*, Coralie Alonso ^*, Jorge Bernardino de la Serna , Jesus Perez-Gil  and H. William Taeusch 

^* Department of Chemical Engineering, University of California, Santa Barbara, California; Bioquimica y Biologia Molecular, Universidad Complutense, Madrid, Spain; and Department of Pediatrics, University of California, San Francisco, California

Correspondence: Address reprint requests to Joseph A. Zasadzinski, Dept. of Chemical Engineering, University of California, Santa Barbara, CA 93106. Tel.: 805-893-4769; Fax: 805-893-4731; E-mail: gorilla{at}engineering.ucsb.edu.

A theory based on the Smolukowski analysis of colloid stability shows that the presence of charged, surface-active serum proteins at the alveolar air-liquid interface can severely reduce or eliminate the adsorption of lung surfactant from the subphase to the interface, consistent with the observations reported in the companion article (pages 1769–1779). Adding nonadsorbing, hydrophilic polymers to the subphase provides a depletion attraction between the surfactant aggregates and the interface, which can overcome the steric and electrostatic resistance to adsorption induced by serum. The depletion force increases with polymer concentration as well as with polymer molecular weight. Increasing the surfactant concentration has a much smaller effect than adding polymer, as is observed. Natural hydrophilic polymers, like the SP-A present in native surfactant, or hyaluronan, normally present in the alveolar fluids, can enhance adsorption in the presence of serum to eliminate inactivation.

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