Feto-placental hypoxemia regulates the release of fetal activin A and prostaglandin E-2

The evaluation of the role of critical hypoxia in unexplained fetal death i n utero has been hampered by the lack of a physiological marker. Here we re port the never observation that fete-placental hypoxemia is an acute trigge r for increased activin secretion from the fete-placental unit in late preg nancy. Hypoxemia was induced in chronically cannulated late pregnant fetal sheep by restricting blood flow through the maternal uterine arteries. Usin g maternal and fetal blood samples and amniotic fluid obtained via chronica lly implanted catheters, fetal blood gas parameters, plasma and amniotic fl uid concentrations of activin A, prostaglandin (PG) E-2 and PGFM, the circu lating metabolite of PGF(2 alpha), were determined before, during and after a ten hour period of fetal hypoxemia. Hypoxemia acutely increased activin A and PGE(2) levels in both amniotic fluid and the fetal circulation with v alues rapidly returning to baseline with normoxemia. PGFM also increased in both compartments with a relatively delayed time frame compared to that of activin A and PGE(2). The increase in activin A and PGE(2) induced by hypo xemia may be a mechanism to regulate fete-placental blood flow during fetal compromise and also offers the possibility that activin A represents a use ful marker of fete-placental hypoxemia.