ANTENATAL GLUCOCORTICOID CORRECTS PULMONARY IMMATURITY IN EXPERIMENTALLY-INDUCED CONGENITAL DIAPHRAGMATIC-HERNIA IN RATS

Congenital diaphragmatic hernia, a highly lethal condition, displays a t term the pulmonary biochemical and morphologic immaturity characteri stic of premature delivery. We hypothesized that antenatal glucocortic oid, now the standard treatment to prevent hyaline membrane disease in premature human beings, might correct the parameters of the pulmonary biochemical and morphologic immaturity in severe congenital diaphragm atic hernia. A total of 112 fetal rats with or without nitrofen-induce d congenital diaphragmatic hernias from 34 pregnancies were treated an tenatally with either saline or dexamethasone. Antenatal dexamethasone increased the lung disaturated phosphatidylcholine content, reduced t he lung glycogen concentration, reduced the saccular septal thickness, and increased the mean saccular size and volume fraction of saccules in the lungs of rats with large congenital diaphragmatic hernia in com parison with similar rats not so treated. All differences were statist ically significant. Antenatal glucocorticoid therapy was efficacious i n treating rats with nitrofen-induced congenital diaphragmatic hernia. This encouraging finding warrants further investigation in a large an imal model with surgically created congenital diaphragmatic hernia.