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Division of Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039
Mice
carrying a null mutation of the surfactant-associated protein A (SP-A)
gene have normal respiratory function, but their surfactant lacks
tubular myelin, is sensitive to protein inactivation in vitro, and
contains decreased pool sizes of the biophysically active
large-aggregate surfactant. We hypothesized that SP-A-deficient mice
would be more susceptible to exercise-induced stress and O2-induced lung injury. SP-A-(
/) and SP-A-(+/+) mice
tolerated 1 h of swimming or 45 min of running on a treadmill at
15 m/min equivalently, without alterations of the amount of alveolar
saturated phosphatidylcholine. After 3 days of hyperoxia, SP-A-(/)
mice had increased alveolar protein, but pressure-volume curves were not different between groups. Alveolar protein concentration was similarly increased in SP-A-(/) and SP-A-(+/+) mice after 4 days of
exposure to hyperoxia. Survival rates were similar after 4 days of
hyperoxia. SP-A-(/) mice were equally tolerant to exercise and 4 days of hyperoxia, indicating that the SP-A-dependent alterations in
surfactant did not result in functional deficits.
saturated phosphatidylcholine; protein permeability; lung injury; pressure-volume curve; surfactant metabolism
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