MATERNAL DEXAMETHASONE TREATMENT ENHANCES THE EXPRESSION OF SURFACTANT APOPROTEIN-A IN THE HYPOPLASTIC LUNG OF RABBIT FETUSES INDUCED BY OLIGOHYDRAMNIOS

Previously the authors reported that oligohydramnios induced lung hypo plasia in rabbit fetuses and showed that sustained oligohydramnios, wh ich was induced by amniotic shunting from gestational sacs into the ma ternal peritoneal cavity between 23 and 30 days' gestation, significan tly retards not only lung structural growth but also the functional de velopment of alveolar type II cells in surfactant apoprotein A (SP-A) expression. In the present study, the authors examined, both immunohis tochemically and morphometrically, whether the maternal administration of dexamethasone restored SP-A synthesis in fetal hypoplastic lungs. The fetal rabbits were treated through maternal administration of dexa methasone (0.25 mg/kg/d) or saline 48 and 24 hours before delivery, at 30 days' gestation. The ratio of lung weight to body weight was signi ficantly greater for the dexamethasone-treated fetuses compared with t he saline-treated fetuses in both the shunted and the nonshunted group s (P < .05). Compared with the lungs of the saline-treated fetuses, th ose of the dexamethasone-treated fetuses had a statistically significa nt increase in SP-A expression, namely the number of SP-A-positive typ e II cells per unit area (P < .001), the ratio of SP-A-positive cells to the total number of cells (P < .01), and the percentage of SP-A-pos itive area per unit area (P < .05) in the shunted group. An increase i n the ratio of SP-A-positive area to lung interstitial was found for t he shunted group. However, similar findings were not observed in the n onshunted group. The results suggest that maternal dexamethasone treat ment accelerates the functional development of alveolar type II cells in SP-A expression, even in hypoplastic lungs induced by oligohydramni os. Copyright (C) 1996 by W.B. Saunders Company