Prostaglandin production by guinea-pig placenta and other uterine tissues during mid-pregnancy

Prostaglandin (PG) output from cultured placenta, sub-placenta, endometrium and fetal membranes of guinea-pigs was measured on days 22, 29 and 36 of pregnancy to establish the source of increased PGF2alpha production during mid-pregnancy. PGF2alpha and 6-keto-PGF1alpha were produced in larger quantities than PGE2 by the placenta, sub-placenta and endometrium; 6-keto-PGF1alpha was in the major prostaglandin produced by the fetal membranes. The initial outputs of PGF2alpha, PGE2 and 6-keto-PGF1alpha from the sub-placenta, fetal membranes and endometrium either decreased or remained fairly constant between days 22 and 36. In contrast, the initial outputs of PGF2alpha, PGE2 and 6-keto-PGF1alpha from the placenta increased 14.7-, 2.5- and 2.0-fold, respectively, between days 22 and 36, indicating that the placenta is the tissue responsible for the increase in PGF2alpha output from the mid-pregnant guinea-pig uterus. Aristolochic acid (a phospholipase A2 inhibitor) inhibited prostaglandin output from the endometrium, but had a more variable effect in prostaglandin output from the other tissues. Thimerosal (an arachidonic acid uptake inhibitor) inhibited PGF2alpha and PGE2 outputs from the endometrium, but generally potentiated 6-keto-PGF1alpha output and prostaglandin output from the other tissues. Arachidonic acid release for prostaglandin synthesis in the endometrium, but not the placenta, sub-placental or fetal membranes, is apparently dependent upon a constant level of phospholipase A2 activity.