| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Division of Neonatal Medicine, Department of Pediatrics, Neonatal-Perinatal Research Institute, Duke University Medical Center, Durham, North Carolina 27710; and 2 Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505
In acute lung injury, a disturbed surfactant
system may impair gas exchange. Previous evaluations of hyperoxia
effects on surfactant proteins (SPs) followed exposures >1-2
days. To evaluate the effects of brief exposure to hyperoxia on
the SP system, we exposed adult male rats to 95%
O2 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
semiquantitative 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 extent on numbers of
positively labeled cells. SP-B declined to 50% of control in lavage at
12 h, but no changes in total lung SP-A and -B were seen. The number of
SP-A positively labeled cells did not change, but SP-A label intensity
measured by IHC in type II cells showed parallel results to Northern
blots and ISH. The response of SP-A in Clara cells was similar. SP-B
immunolabeling intensity rose in both type II and Clara cells
throughout the exposure. 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%
O2 and may affect local alveolar stability.
lung injury; in situ hybridization; hyperoxia
This article has been cited by other articles:
|
|
 |
|
  M. Ikegami, A. Falcone, and J. A. Whitsett STAT-3 regulates surfactant phospholipid homeostasis in normal lung and during endotoxin-mediated lung injury J Appl Physiol, June 1, 2008; 104(6): 1753 - 1760. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. L. Auten, M. A. O'Reilly, T. D. Oury, E. Nozik-Grayck, and M. H. Whorton Transgenic extracellular superoxide dismutase protects postnatal alveolar epithelial proliferation and development during hyperoxia Am J Physiol Lung Cell Mol Physiol, January 1, 2006; 290(1): L32 - L40. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. B. Stuart, B. Ovadia, V. V. Suzara, P. A. Ross, S. Thelitz, J. R. Fineman, and J. A. Gutierrez Inhaled nitric oxide increases surfactant protein gene expression in the intact lamb Am J Physiol Lung Cell Mol Physiol, September 1, 2003; 285(3): L628 - L633. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. N. Ahmed, H. B. Suliman, R. J. Folz, E. Nozik-Grayck, M. L. Golson, S. N. Mason, and R. L. Auten Extracellular Superoxide Dismutase Protects Lung Development in Hyperoxia-exposed Newborn Mice Am. J. Respir. Crit. Care Med., February 1, 2003; 167(3): 400 - 405. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. L. Auten Jr., S. N. Mason, D. T. Tanaka, K. Welty-Wolf, and M. H. Whorton Anti-neutrophil chemokine preserves alveolar development in hyperoxia-exposed newborn rats Am J Physiol Lung Cell Mol Physiol, August 1, 2001; 281(2): L336 - L344. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
