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Prostaglandin E2 tablets were administered intravaginally 505 patients for the induction of labour, without amniotomy, using doses ranging from 1 to 5 mg as a single insertion. The advantages and limitations of this method of induction of labour are discussed.
Serial plasma samples collected before and after vacuum curettage followed by methylergometrine injection in 10 women were assayed for 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha). The mean 6-keto-PGF1 alpha concentration was 97.2 (SE 8.8) pg/ml before cervical dilatation. The concentration rose to 128.2 (SE 13.5) pg/ml (P less than 0.10) immediately and to 133.3 (SE 17.8) pg/ml (P less than 0.05) 1 h after curettage and returned to the initial value within 5 h. Neither methylergometrine nor anaesthesia, nor non-gynaecological surgery, caused changes in the level of plasma 6-keto-PGF1 alpha. The capacity of the platelets to produce thromboxane A2 during spontaneous clotting of blood did not change during vacuum curettage, anaesthesia and non-gynaecological surgery, nor after methylergometrine. The evidence suggests that the pregnant myometrium and/or intrauterine tissues capable of generating prostacyclin (PGI2) in vitro may release PGI2 also in vivo.
A double-blind placebo-controlled trial was performed in 20 primigravidae to assess the physiological and clinical effects of oral mifepristone on myometrial contractility and sensitivity in the second trimester. Ten women received 600 mg of oral mifepristone and 10 women a placebo 24 h before abortion was induced in both groups, with extra-amniotic PGE2 instillation. Intrauterine pressure recordings demonstrated increased spontaneous uterine activity and increased sensitivity to PGE2 and ergometrine, but no change in oxytocin sensitivity after mifepristone treatment. There were no significant differences in PGE or PGF metabolite concentrations in peripheral maternal plasma over the 24-h study period after treatment between the mifepristone and placebo groups. The mean induction abortion interval in the mifepristone group was 512 (SD 321) min compared with 1128 (SD 606) min in the placebo group (P less than or equal to 0.02). The mechanism whereby mifepristone provokes enhanced uterine contractility and sensitivity to prostaglandins, with a reduction in abortion times, does not appear to be through endogenous production of PGE or PGF.
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Catheters were implanted into 16 ewes and their foetuses between days 110 and 124 of gestation. Hypophysectomy was attempted in eight of these foetuses. Continuous infusion of synthetic ACTH (10 microgram/h) or dexamethasone (1mg/24 h) into the foetus, starting between days 124 and 129, induced premature parturition. The concentration of progesterone in the maternal peripheral plasma decreased before parturition in all animals while the level of oestradiol increased in ewes with intact foetuses or in those in which hypophysectomy was incomplete. When hypophysectomy was complete, no increase in the maternal level of oestradiol occurred before delivery. The concentration of 13,14-dihydro-15-oxo-prostaglandin F2alpha increased in the peripheral plasma of ewes with intact or hypophysectomized foetuses infused with ACTH. It is suggested that an intact foetal pituitary gland is required for the rise in the level of oestrogen prepartum, but that this rise is not essential for increased prostaglandin production of parturition.
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The effect of a single dose of RU 486 (600mg) on prostaglandin metabolite levels has been studied over a 48 h period in 20 women undergoing medical termination of early pregnancy. The results were compared with controls of similar gestation who were treated surgically. The mean (SD) PGEM levels at 0 and 48 h in the RU 486 group were 13.7 (2.7) and 13.2 (2.2) pg/ml respectively, which was not significantly different from the values of 11.7 (1.1) and 11.3 (0.4) pg/ml measured in the control patients. Similarly the mean (SD) PGFM values of 22.3 (14.7) and 17.0 (7.2) pg/ml at 0 and 48 h were not significantly different from the corresponding control values of 21.9 (13.8) and 23.8 (7.2) pg/ml. In 10 of the study patients, there were no significant changes in PGEM and PGFM concentrations prior to and at 4, 24 and 48 h after RU 486 administration. Although all pregnancies were successfully terminated with the combination of RU 486 and subsequently a vaginal pessary containing PGE1, no stimulation of prostaglandin production could be demonstrated.
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The prostaglandin synthetase inhibitor ibuprofen was evaluated for relief of severe primary dysmenorrhea in a controlled, double-blind, cross-over study in seven patients for a total of 23 menstrual cycles. In eight untreated cycles, the amount of prostaglandin (PG) in the menstrual fluid was higher than in nondysmenorrheic subjects. There was good to excellent relief of dysmenorrhea in seven ibuprofen-treated cycles, which was associated with a threefold to fourfold reduction in menstrual PG released. When a placebo was given in five cycles, only poor or minimal relief of dysmenorrhea was obtained and the menstrual PG released was similar to that in control cycles. In individual patients, there was a remarkable correlation between the severity of menstrual pain as assessed daily by the patient and the level of menstrual PG released during the corresponding period. The effect of ibuprofen therapy on menstrual fluid volume was inconsistent. The study shows that in severe primary dysmenorrhea there is increased release of PG in the menstrual fluid; this can be effectively suppressed with ibuprofen, which provides excellent relief from the symptoms of dysmenorrhea.