| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||

* Departments of Chemical Engineering and Materials, University of California, Santa Barbara, California 93106-5080; and
Department of Pediatrics, Los Angeles Biomedical Research Institute at Harbor UCLA Medical Center, Torrance, California 90502, and Department of Medicine, University of California, Los Angeles, California 90095
Correspondence: Address reprint requests to Joseph A. Zasadzinski, Tel.: 805-893-4769; Fax: 805-893-4731; E-mail: gorilla{at}engineering.ucsb.edu.
Lung surfactant causes the surface tension,
, in the alveoli to drop to nearly zero on exhalation; in the upper airways
is
30 mN/m and constant. Hence, a surface tension gradient exists between alveoli and airways that should lead to surfactant flow out of the alveoli and elimination of the surface tension gradient. However, the lung surfactant specific protein SP-C enhances the resistance to surfactant flow by regulating the ratio of solid to fluid phase in the monolayer, leading to a jamming transition at which the monolayer transforms from fluidlike to solidlike. The accompanying three orders of magnitude increase in surface viscosity helps minimize surfactant flow to the airways and likely stabilizes the alveoli against collapse.
This article has been cited by other articles:
![]() |
M. Saleem, M. C. Meyer, D. Breitenstein, and H.-J. Galla The Surfactant Peptide KL4 in Lipid Monolayers: PHASE BEHAVIOR, TOPOGRAPHY, AND CHEMICAL DISTRIBUTION J. Biol. Chem., February 22, 2008; 283(8): 5195 - 5207. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |