Abstract
Intrauterine fetal growth restriction (IUGR) is associated with high rates of neonatal morbidity. IUGR babies are often born preterm and are therefore exposed to antenatal glucocorticoids. Antenatal glucocorticoids significantly improve overall survival rates of preterm infants, but there is a paucity of information about their effects on IUGR infants. We induced IUGR in sheep by single umbilical artery ligation (SUAL), or sham in control fetuses. To half the ewes, we administered betamethasone (BM) on days 5 (BM1) and 6 (BM2) following surgery and collected fetal lung tissue on day 7. SUAL alone was associated with higher circulating fetal cortisol levels (2.8+/-0.4 vs 1.0+/-0.4, P=0.001) compared to controls, but no changes in lung morphology or surfactant protein (SP) gene expression. BM was associated with a significant reduction in lung tissue density (P=0.048). There were no significant differences between groups in lung DNA concentration or septal crest density. SP-A, -B and -C gene expression was significantly increased in control and SUAL fetuses given BM. These results show that in SUAL fetuses, maternal betamethasone is associated with acceleration of fetal lung structure, as occurs in normally grown fetuses, and that betamethasone induces SP production, an effect not observed in SUAL-induced IUGR fetuses alone.
Original language | English |
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Pages (from-to) | 689 - 696 |
Number of pages | 8 |
Journal | Pediatric Research |
Volume | 71 |
Issue number | 6 |
DOIs | |
Publication status | Published - 2012 |