The effect of prenatal glucocorticoid treatment on levels of immunoreactive 6-ketoprostaglandin F,1α(PGF1α) (the stable metabolite of prostacyclin) was studied in fetal rat lungs. During late gestation (20-22 days), levels of 6-keto-PGF1α peaked at 21 days in offspring of control mothers. At a maternal dose of 0.2 mg/kg dexamethasone, maximal enhancement of fetal 6-keto-PGF1α levels occurred at 20 days gestation. At a treatment dose of 0.4 mg/kg, however, dexamethasone increased fetal lung 6-keto-PGF1α concentrations throughout late gestation. Because maturation of fetal lung is known to be delayed in males relative to females, we also studied the impact of sex of the fetus on levels of 6-keto-PGF1α. Our results showed no statistically significant differences between females and males in any of the treatment groups at an of the gestational ages studied. These results suggest that prenatal dexamethasone enhances endogenous levels of 6-keto-PGF1α in fetal rat lungs. Since prostacyclin may play important roles in fetal lung maturation and neonatal lung function, the effectiveness of prenatal glucocorticoid therapy for accelerating functional maturity of the fetal lung may in part be due to stimulation of prostacyclin synthesis.