The Regulation of Arachidonic Acid Release in Parturition

Abstract

One of the rate limiting steps in prostaglandin biosynthesis is the release of free arachidonic acid (1,2). In the present investigation is described the results of a study in which: 1) we have defined the lipid species of the human fetal membranes that serves as the source of arachidonic acid for prostaglandin biosynthesis during human parturition; 2) we have defined the enzymatic mechanism involved in this release; 3) we have investigated the regulation of these processes with special emphasis on the possible inter-relationship between the fetal lung and fetal membranes, to the initiation of parturition. Several years ago we observed that the concentration of arachidonic acid increased disproportionally in human amniotic fluid during labor (3). It has been reported by numerous investigators that prostaglandins are produced in large amounts by uterine and intra-uterine tissues during parturition. We also demonstrated that the microsomal fraction prepared from several intra-uterine tissues, including amnion, and chorion laeve, had a high capacity for prostaglandin formation from arachidonic acid (4). We suggested that the source of the arachidonic acid was fetal membranes.