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Prostaglandin F2α, oxytocin and uterine activation in hypertonic saline-induced abortions

1984; Elsevier BV; Volume: 150; Issue: 1 Linguagem: Inglês

10.1016/s0002-9378(84)80104-0

1097-6868

Anna‐Riitta Fuchs, Anne B. Rasmussen, Jaana Rehnström, Miklós Tóth,

Maternal and fetal healthcare

Intra-amniotic injections of hypertonic saline at midgestation induce uterine activity, which evolves into a laborlike pattern in less than 24 hours and is associated with progressive increase in uterine oxytocin response. This uterine activation occurred in the absence of a measurable increase in plasma 13,14-dihydro-15-keto-prostaglandin F2α (PGFM). Only after 25 to 27 hours was a rise in plasma concentration of PGFM detected, which then increased in a parallel manner with cervical dilatation. By contrast, plasma oxytocin levels increased by almost 100% soon after the injection of hypertonic saline, declining to initial levels by 24 to 28 hours. Oxytocin infusions given after the intra-amniotic injection at rates resulting in about a fivefold increase in plasma oxytocin significantly accelerated cervical dilatation and the rise in plasma PGFM. Oxytocin infused before induction of abortion resulted in only a small and transient rise in plasma PGFM. Hypertonic saline injections thus increase the prostaglandin F2α-stimulating action of oxytocin, which in turn may be responsible for the enhanced contractile response to the hormone. Myometrial activation after hypertonic saline injections is probably caused by an interaction of oxytocin and prostaglandin F2α, and cervical dilatation depends on contractile activity and a critical increase in prostaglandin production. Intra-amniotic injections of hypertonic saline at midgestation induce uterine activity, which evolves into a laborlike pattern in less than 24 hours and is associated with progressive increase in uterine oxytocin response. This uterine activation occurred in the absence of a measurable increase in plasma 13,14-dihydro-15-keto-prostaglandin F2α (PGFM). Only after 25 to 27 hours was a rise in plasma concentration of PGFM detected, which then increased in a parallel manner with cervical dilatation. By contrast, plasma oxytocin levels increased by almost 100% soon after the injection of hypertonic saline, declining to initial levels by 24 to 28 hours. Oxytocin infusions given after the intra-amniotic injection at rates resulting in about a fivefold increase in plasma oxytocin significantly accelerated cervical dilatation and the rise in plasma PGFM. Oxytocin infused before induction of abortion resulted in only a small and transient rise in plasma PGFM. Hypertonic saline injections thus increase the prostaglandin F2α-stimulating action of oxytocin, which in turn may be responsible for the enhanced contractile response to the hormone. Myometrial activation after hypertonic saline injections is probably caused by an interaction of oxytocin and prostaglandin F2α, and cervical dilatation depends on contractile activity and a critical increase in prostaglandin production.