Maternal dexamethasone treatment enhances the expression of surfactant apoprotein A in the hypoplastic lung of rabbit fetuses induced by oligohydramnios.
A previous study documented the effects of maternal corticosteroid treatment on structural growth and functional development in fetal lungs associated with pathogenic conditions such as oligohydramnios using immunohistochemical and morphometric analyses. The purpose of the present study was to examine the effect of maternal dexamethasone treatment the expression of lamellar body in type II pneumocytes of the fetal rabbit lungs with hypoplasia induced by oligohydramnios using electron microscopy. Using an amniotic shunting rabbit model, pregnant rabbits were injected intravenously with either 0.1 ml of saline or 0.25 mg/kg/day of dexamethasone in 0.1 ml of saline 48 and 24 h before the delivery of fetuses, at day 30 of gestation. The number of lamellar bodies per type II pneumocyte was counted in each group using electron micrographs. The number of lamellar bodies per type II pneumocyte in the lungs of the shunted group that received saline was consistently and significantly less than that of the other three groups (5.49 ± 2.07 vs. 7.34 ± 2.27: shunted group that received dexamethasone, 7.58 ± 2.08: non-shunted group that received saline, 7.79 ± 1.90: non-shunted group that received dexamethasone; P < 0.01). These results suggest that maternal dexamethasone treatment accelerates the maturation of the surfactant system, especially the expression of lamellar bodies in type II pneumocytes, even in hypoplastic lungs induced by oligohydramnios.