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

Abstract

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 PGF 2α production during mid-pregnancy. PGF 2α and 6-keto-PGF 1α were produced in larger quantities than PGE 2 by the placenta, sub-placenta and endometrium; 6-keto-PGF 1α was in the major prostaglandin produced by the fetal membranes. The initial outputs of PGF 2α, PGE 2 and 6-keto-PGF 1α 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 PGF 2α, PGE 2 and 6-keto-PGF 1α 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 PGF 2α output from the mid-pregnant guinea-pig uterus. Aristolochic acid (a phospholipase A 2 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 PGF 2α and PGE 2 outputs from the endometrium, but generally potentiated 6-keto-PGF 1α 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 A 2 activity.