Journal of Applied Physiology
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J Appl Physiol 89: 644-648, 2000;
8750-7587/00 $5.00
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Vol. 89, Issue 2, 644-648, August 2000

Tolerance of SP-A-deficient mice to hyperoxia or exercise

Machiko Ikegami, Alan H. Jobe, Jeffrey Whitsett, and Thomas Korfhagen

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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