Tolerance of SP-A-deficient mice to hyperoxia or exercise
Tolerance of SP-A-deficient mice to hyperoxia or exercise
复制标题
DOI：
10.1152/jappl.2000.89.2.644
复制
发表时间：
2000-08-01
影响因子：
3.3
通讯作者：
Korfhagen, T
中科院分区：
文献类型：
--
作者：
Ikegami, M;Jobe, AH;Korfhagen, T
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 O-2-induced lung injury. SP-A-(-/-) and SP-A-(+/+) mice tolerated Ih 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.
