Abstract
Prenatal Glucocorticoid therapy is increasingly being used for accelerating fetal lung maturation. Glucocorticoids, however, are also known to inhibit phospholipase A2 and thus the synthesis of prostaglandins(PG). In perinatal rat lung, the major PG is prostacyclin(PGI2), a potent vaso- and bronchodilator important in lung function. To determine the effect of gluococorticoid therapy on fetal lung PGI2 synthesis, we measured 6-keto-PGF1α (the stable breakdown product of PGI2) levels by RIA. Pregnant rats received 4 doses of dexamethasone(DEX)(0.4mg/kg) at 12hr intervals prior to sacrifice. Table 1 shows the 6-keto-PGF1α levels of fetal lungs from DEX-treated and control mothers (mean ± SEM, 4 fetuses from each of 6 litters for each group).
DEX treatment significantly increased 6-keto-PGF1α levels. There were no significant differences between male and female fetuses with or without DEX treatment. GC/MS studies confirmed results obtained by RIA. These results suggest that prenatal DEX enhances endogenous levels of 6-keto-PGF1α in fetal lung. Since PGI2 may be important in perinatal lung maturation and function, the effectiveness of glucocorticoid therapy for accelerating functional lung maturity may be partly due to the stimulation of PGI2 synthesis.
Article PDF
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Tsai, M., Josephson, M., Handschin, B. et al. Effect of Prenatal Glucocorticoid on Fetal Rat Lung Prostaglandin Synthesis. Pediatr Res 18 (Suppl 4), 352 (1984). https://doi.org/10.1203/00006450-198404001-01553
Issue Date:
DOI: https://doi.org/10.1203/00006450-198404001-01553