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

Abstract

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.