Abstract
A significant increment of the release of decidual prolactin (d-PRL) was observed when human decidual tissue was incubated with 10-5M cortisol (F) . However, stimulation by F was diminished by the addition of actinomycin-D. Addition of dehydroepiandrosterone (DHA), DHA-S, estradiol (E2), estriol or beta-methasone did not affect the release of decidual PRL. Eight pregnant women (38-40 weeks gestation) complicated with bronchial asthma were administered 4 mg of beta-methasone, intravenously, 4 hours prior to cesarean section. Maternal venous (MV), umbilical arterial (UA) and umblical venous (UV) blood, and amniotic fluid (AF) and decidual tissue were obtained during cesarean section. PRL, DHA, DHA-S and F values were measured by RIA and were compared with those obtained from controls. Release of PRL into the medium from the decidua was also studied. It was found that PRL levels in MV and AF were significantly lower for patients who received beta-methasone than for the controls, but there were no differences in UA nor UV. F levels in all sources decreased in the treated patients. DHA levels in MV, UA and UV also decreased, and DHA-S levels in MV, UA and AF were found to be lower in the treated patients than in the controls. Release of PRL from decidual tissue obtained from the treated patients, into the medium was lower than that from control tissue. The results indicate that treatment for pregnant woman at term with glucocorticoid suppresses both maternal and fetal pituitary-adrenal functions, which consequently decreases the secretion of steroid including estrogen. Changes of steroid profile may result in changes of PRL levels. An in vitro experiment using decidual tissue demonstrated that the release of d-PRL was stimulated by F, indicating the physiological significance of steroids circulating in the feto-placento-maternal compartment for the control of d-PRL production.
