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Prenatal glucocorticoids improve lung morphology and partially restores surfactant mRNA expression in lambs with diaphragmatic hernia undergoing fetal tracheal occlusion
Author(s) -
Davey Marcus G.,
Danzer Enrico,
Schwarz Uwe,
Robinson Lauren,
Shegu Shincy,
Adzick N. Scott,
Flake Alan W.,
Hedrick Holly L.
Publication year - 2006
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.20516
Subject(s) - congenital diaphragmatic hernia , fetus , lung , medicine , diaphragmatic hernia , betamethasone , lung volumes , andrology , endocrinology , hernia , surgery , pregnancy , biology , genetics
In fetal sheep with surgically created diaphragmatic hernia (DH), tracheal occlusion (TO) can restore lung growth but does not ameliorate the increase in inter‐alveolar wall thickness (T W ).1 We determined whether prenatal exposure to glucocorticoids (GC) could reduce T w in fetuses with DH undergoing TO. At 65 days of gestation, DH was created in 12 fetal sheep, and TO subsequently performed at 110 days (DH/TO). Six of these fetuses were exposed to betamethasone (DH/TO + GC; 0.5 mg/kg; maternal, IM) 48 hr before delivery; Sham operated fetuses (n = 7) served as controls. At 139 days, we measured alveolar surface density (S V ), parenchymal tissue fraction, T W , alveolar type 2 (AE2) cell density and lung surfactant protein (SP) mRNA expression. Prenatal GC decreased T W and S V by 33% and 27% respectively, and increased fixed lung volume (by 55%), AE2 cell density and partially restored SPmRNA expression. Our data indicate that prenatal exposure to GC can reverse some of the negative effects of prolonged fetal TO. We hypothesize that a GC‐induced reduction in lung liquid volume during TO contributes, in part, to the observed increase in AE2 cell density and SPmRNA expression. Pediatr Pulmonol. 2006; 41:1188–1196. © 2006 Wiley‐Liss, Inc.

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