Abstract
Summary: Injection of 11-ketoprogesterone into fetal rats at day 17 of gestation reduced the pulmonary C-11 activation index (an indicator of net gain or loss of glucocorticoid activity) as measured at day 21 (P < 0.001) and resulted in elevated levels of the inactive hormone 11-dehydrocorticosterone (P < 0.001), but unchanged corticosterone levels. Adrenal weight was significantly increased (P < 0.001). 11-Ketoprogesterone-injected fetuses had considerably larger lungs (P < 0.001) with reduced saturated phosphatidylcholine content (P < 0.001). Speculation: Prenatal glucocorticoid treatment to accelerate fetal lung maturation is an attempt to mimic a physiologic process. Further understanding of that process should provide means to enhance the safety and efficacy of such therapeutic intervention.