Estradiol added to tissue culture or intraamniotic installation of dehydroepiandrosterone sulfate (which increases amniotic fluid estradiol levels several-fold) had no effect on am-niotic fluid prolactin concentrations. Arachidonic acid, which stimulates the release of pituitary prolactin, inhibits both the basal release and the increase in decidual prolactin in response to PRL-RF.
The action of arachidonic acid is apparently not secondary to conversion to eicosanoid products since cyclooxygenase and lipoxygenase inhibitors did not alter this response, although higher doses of indomethacin and flufenamic acid caused an inhibition of basal secretion of prolactin from decidual explants. Our results showing that indomethacin blocked the stimulatory effects of IL-ip infusion on amniotic fluid PG concentrations, but not the decline in amniotic fluid prolactin, are consistent with the findings of Handwerger et al.. Moreover, the decrease in amniotic fluid prolactin with infection is not due to a nonspecific effect of widespread decidual necrosis nor to an effect of maternal, fetal, or amniotic fluid progesterone, which actually increased prior to delivery after infection (see Table 3). buy ampicillin