Brief 95% O-2 exposure effects on surfactant protein and mRNA in rat alveolar and bronchiolar epithelium

Citation
Tf. Allred et al., Brief 95% O-2 exposure effects on surfactant protein and mRNA in rat alveolar and bronchiolar epithelium, AM J P-LUNG, 20(6), 1999, pp. L999-L1009
Citations number
35
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
ISSN journal
10400605 → ACNP
Volume
20
Issue
6
Year of publication
1999
Pages
L999 - L1009
Database
ISI
SICI code
1040-0605(199906)20:6<L999:B9OEEO>2.0.ZU;2-D
Abstract
In acute lung injury, a disturbed surfactant system may impair gas exchange . Previous evaluations of hyperoxia effects on surfactant proteins (SPs) fo llowed exposures >1-2 days. To evaluate the effects of brief exposure to hy peroxia on the SP system, we exposed adult male rats to 95% O-2 or air for 12, 36, and 60 h. SP-A, -B, and -C mRNAs were analyzed by Northern blot and semiquantitative in situ hybridization (ISH). SP-A and -B were analyzed in whole lung homogenates, lung lavage fluid, and fixed tissue by semiquantit ative immunohistochemistry (IHC). All SP mRNAs were diminished at 12 h and rose to or exceeded control by 60 h as determined by Northern blot and ISH. These effects were seen mainly in the intensity of ISH signal per cell in both type II and bronchiolar epithelial (Clara) cells and to a lesser exten t on numbers of positively labeled cells. SP-B declined to 50% of control i n lavage at 12 h, but no changes in total lung SP-A and -B were seen. The n umber of SP-A positively labeled cells did not change, but SP-A label inten sity measured by IHC in type II cells showed parallel results to Northern b lots and ISH. The response of SP-A in Clara cells was similar. SP-B immunol abeling intensity rose in both type II and Clara cells throughout the expos ure. SP-C ISH intensity fell at 12 h and was increased to two times control by 60 h of hyperoxia. Sharp declines in SP expression occurred by 12 h of 95% O-2 and may affect local alveolar stability.