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Summary.Intrauterine pressure changes were monitored in 5 pregnant ewes and uterine venous prostaglandin (PG) F concentrations were determined after distension of the vagina. Uterine contractility and utero-ovarian PGF concentrations were elevated by vaginal distension and the magnitude of both effects increased as parturition approached.

Summary.The concentration of thromboxane (TX) B-2 was similar in plasma from all sources but was significantly greater (P< 0·01) in amniotic fluid. Fetal hypophysectomy was without effect on maternal or fetal levels of TXB-2 (P> 0·1). Neither normal parturition at term nor prematurely induced delivery was associated with any significant trend in TXB-2 levels. During late pregnancy (105–145 days of gestation) the concentrations of TXB-2 and 13, 14-dihydro-15-keto-prostaglandin F (PGFM) in maternal and fetal plasma were significantly correlated (P< 0·001). There was, however, no correlation between TXB-2 and PGFM levels in samples taken during the 36 h before delivery. These data suggest that thromboxanes play little part in the mechanism of parturition in sheep.

Summary.After extra-amniotic treatment of pregnant rhesus monkeys premature parturition was induced in 4 given 2·5 mg PGE-2; none of the 4 monkeys given 100 mg arachidonic acid were affected. The concentrations of PGE, PGF or 13,14-dihydro-15-oxo-PGF did not change after arachidonic acid treatment, but all increased after PGE-2. It is suggested that the availability of substrate, arachidonic acid, is not a major factor governing the control of PG synthesis but that the latter is suppressed during pregnancy.

Summary.15-Hydroxyprostaglandin dehydrogenase (PGDH) was measured in vitroin myometrium and maternal cotyledons from 6 sheep and in fetal cotyledons from 3 sheep before and after parturition. Maternal cotyledons contained more PGDH than fetal cotyledons or myometrium. At parturition, PGDH activity decreased in myometrium but increased in fetal and maternal placental tissue. The enzymatic activity observed in vitrodid not result in a large, consistent release of prostaglandin F metabolites into the utero-ovarian vein in vivo, and such activity may have a strictly localized effect in ovine parturition.

Summary.Plasma samples were obtained from 8 conscious rhesus monkeys at 3–4 day intervals throughout the menstrual cycle. Oxytocin concentrations were significantly higher in mid-cycle (Days 10–11) than at Days 4–5 (P< 0·01) and Days 28–29 (P< 0·02, Wilcoxon signed rank test). No significant correlations between oxytocin and oestradiol or progesterone were found.

Summary.Active immunization of sheep against oxytocin prolonged the luteal phase of the oestrous cycle, as judged by oestrous behaviour and circulating progesterone concentrations. Mean cycle length was extended by 3·7 days. The treatment resulted in a 10-fold increase in circulating oxytocin concentrations. Antisera produced were specific for oxytocin; cross-reactions with vasotocin, arginine vasopressin, and hypothalamic releasing factors were low. Cerebrospinal fluid contained low levels of antibodies directed against oxytocin. This finding supports the hypothesis that the luteolytic action of oestradiol-17β in sheep may be mediated through a stimulatory effect on the endometrial oxytocin receptor concentration.

Summary.Prostaglandins (PG) E and F, and 13,14-dihydro-15-keto-prostaglandin F (PGFM) were measured in plasma collected from the umbilical artery and vein, the maternal carotid artery, and the utero-ovarian vein of pregnant sheep between 116 and 139 days of gestation. PGE levels were greater than PGF levels in the umbilical artery and vein and the maternal carotid artery, but not in the utero-ovarian vein. PGFM exceeded PGF in samples from all vessels. There was a significant vein-to-artery concentration difference for PGF and PGFM, but not for PGE, in the umbilical circulation. Utero-ovarian concentrations of all 3 PGs generally exceeded their concentrations in the maternal carotid artery.

To investigate the rôle of oxytocin in the increase in utero-ovarian venous prostaglandin F (PGF) level caused by vaginal distension, jugular venous oxytocin and utero-ovarian venous PGF were measured simultaneously in one sheep in late pregnancy and in one sheep shortly before parturition. Vaginal distension raised oxytocin and PGF levels in both animals and oxytocin levels increased before those of PGF. These findings support the suggestion that the elevated PGF levels resulting from vaginal distension are caused by the reflex secretion of oxytocin.