Abstract
The role of PGs in the maintenance and the control of fetal and placental hemodynamics was suggested. Umbilical vessels having smooth muscle that is not innervated may be particularly responsive to vasoactive agents such as PGs. Six UA were freshly obtained from normal term pregnancies. Biosynthesis of PGE2, PGF2α, thromboxane A2 (analyzed as TxB2) and prostacyclin (PGI2) (Measured as 6-keto PGF1α) was studied by incubating UA microsomes with (14C) arachidonic acid (AA) and with (14C) cyclic PG endoperoxide (PGH2), separation by thin layer chromatography and scintillation counting. Percent recovery of (14C) AA and (14C) PGH2 as PGs was 1.73 and 36.4 respectively. The relative percent PGs recovered was (x ± SEM): In addition, PGI2 synthesis by UA microsomes was determined by the degree of inhibition of platelet aggregation compared with inhibition by known PGI2 standards and was 7μg/mg protein. Azo analog I inhibited PGs biosynthesis in duplicate incubations. The results suggest that PGs synthesis by the vascular wall of the UA may contribute to the regulation of vascular tone and platelet vessel wall interaction, thus, modulating fetoplacental blood flow. PGs inhibitors may alter balanced homeostasis in the fetus and the placenta.
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