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The changes with time in intrauterine tissue production and concentrations of PGE-2, PGF-2 alpha, 6-keto PGF-1 alpha and PGFM (13,14-dihydro-15-keto PGF-2 alpha) in maternal and fetal plasma and amniotic fluid were investigated during the first 72 h of pulsatile administration of ACTH1-24 to chronically catheterized fetal sheep. By 72 h there were no changes in the frequency, maximum amplitude or duration of uterine contractions compared to preinfusion values. Basal concentrations of PGE-2 in maternal and fetal plasma were generally higher than those of PGF-2 alpha, while 6-keto PGF-1 alpha values were intermediate. The concentrations of all PGs increased in amniotic fluid during ACTH infusion. In fetal plasma and in maternal vena caval plasma, however, there were significant increases only in PGF-2 alpha and PGFM. No changes were observed in plasma concentrations for any PG during saline infusion. The mean output of PGE-2, PGF-2 alpha and 6-keto PGF-1 alpha by dispersed cells prepared from chorioallantois and fetal and maternal cotyledons was consistently higher after ACTH for 72 h than from saline-infused animals, although significance (P less than 0.05) was achieved only for PGE-2 in chorioallantois . There are 3 conclusions. (1) Increases in ovine intrauterine tissue PG production precede the occurrence of increased myometrial contractile activity after ACTH treatment of fetal sheep. The results imply a causal relationship between rising PG and later myometrial contractions, rather than PG changes resulting from enhanced uterine activity. (2) The major site(s) of increased PG output in vitro from endogenous precursors are fetal structures, especially the chorio-allantoic membranes. (3) Although PGE-2 may be the major circulating PG during late gestation, there is a selective increase in plasma PGF-2 alpha concentrations before the onset of delivery.

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Early changes in prostaglandin concentrations in ovine maternal and fetal plasma, amniotic fluid and from dispersed cells of intrauterine tissues before the onset of ACTH-induced pre-term labour