Effect of prenatal dexamethasone on immunoreactive 6-ketoprostaglandin F1 alpha levels in fetal rat lungs.
The effect of prenatal glucocorticoid treatment on levels of immunoreactive 6-ketoprostaglandin F1 alpha (PGF1 alpha) (the stable metabolite of prostacyclin) was studied in fetal rat lungs. During late gestation (20-22 days), levels of 6-keto-PGF1 alpha 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-PGF1 alpha levels occurred at 20 days gestation. At a treatment dose of 0.4 mg/kg, however, dexamethasone increased fetal lung 6-keto-PGF1 alpha 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-PGF1 alpha. Our results showed no statistically significant differences between females and males in any of the treatment groups at any of the gestational ages studied. These results suggest that prenatal dexamethasone enhances endogenous levels of 6-keto-PGF1 alpha 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.
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism*; D000818:Animals; D002851:Chromatography, High Pressure Liquid; D002855:Chromatography, Thin Layer; D003907:Dexamethasone / Q000494:pharmacology*; D005260:Female; D005325:Fetal Organ Maturity / Q000187:drug effects; D005333:Fetus / Q000187:drug effects; D006801:Humans; D007231:Infant, Newborn; D008168:Lung / Q000196:embryology* / Q000378:metabolism; D008297:Male; D011247:Pregnancy; D011863:Radioimmunoassay; D051381:Rats; D011919:Rats, Inbred Strains; D012127:Respiratory Distress Syndrome, Newborn / Q000517:prevention & control
D015121:6-Ketoprostaglandin F1 alpha; D003907:Dexamethasone