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 hypoplasia in rabbit fetuses and showed that sustained oligohydramnios, which was induced by amniotic shunting from gestational sacs into the maternal peritoneal cavity between 23 and 30 days' gestation, significantly retards not only lung structural growth but also the functional development of alveolar type II cells in surfactant apoprotein A (SP-A) expression. In the present study, the authors examined, both immunohistochemically 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 dexamethasone (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 significantly greater for the dexamethasone-treated fetuses compared with the saline-treated fetuses in both the shunted and the nonshunted groups (P < .05). Compared with the lungs of the saline-treated fetuses, those of the dexamethasone-treated fetuses had a statistically significant increase in SP-A expression, namely the number of SP-A-positive type 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-positive area per unit area (P < .05) in the shunted group. An increase in the ratio of SP-A-positive area to lung interstitial was found for the shunted group. However, similar findings were not observed in the nonshunted group. The results suggest that maternal dexamethasone treatment accelerates the functional development of alveolar type II cells in SP-A expression, even in hypoplastic lungs induced by oligohydramnios.