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MATERNALLY ADMINISTERED DEXAMETHASONE TRANSIENTLY INCREASES APOPTOSIS IN LUNGS OF FETAL RATS

In late gestation, morphological maturation of fetal lung includes septal thinning of potential airspaces, a process accelerated by exogenous glucocorticoids. Apoptosis occurs in normal fetal lung. Glucocorticoids increase apoptosis in several tissues. The authors hypothesized that exogenous glucoco...

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Bibliographic Details
Published in:Experimental lung research 2003-06, Vol.29 (4), p.211-226
Main Authors: Scavo, Louis M., Newman, Valerie, Ertsey, Robert, Chapin, Cheryl J., Kitterman, Joseph A.
Format: Article
Language:English
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Summary:In late gestation, morphological maturation of fetal lung includes septal thinning of potential airspaces, a process accelerated by exogenous glucocorticoids. Apoptosis occurs in normal fetal lung. Glucocorticoids increase apoptosis in several tissues. The authors hypothesized that exogenous glucocorticoids would increase apoptosis in fetal lung, primarily in the interstitium. They administered dexamethasone (DEX), 1 mg/kg, or vehicle (Control) to pregnant rats at 19 days of gestation. Fetuses were delivered at 3, 7, 12, or 24 hours post injection. DEX decreased fetal body weight and lung weight, DNA, and protein 12 hours post injection. Using the terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) reaction to label apoptotic cells in lung, they calculated an apoptotic index (AI, apoptotic cells/1000 total cells) for each fetus. Average DEX AI (3.6 ± 2.6, mean ± SD) was greater than Control (1.7 ± 0.5) (P
ISSN:0190-2148
1521-0499
DOI:10.1080/01902140303784