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Biomedical subjects

A R Fuchs

Publications and source records attributed to A R Fuchs.

At least 73 records · Page 4Linked to original sources

Release of oxytocin and prolactin by suckling in rabbits throughout lactation.

Plasma oxytocin and PRL were measured in serial samples of blood collected from lactating rabbits nursing five to seven (mean, six) young on a once-daily suckling regimen. Each suckling episode lasted 4.0 +/- 1.1 (+/- SD) min on the average. Samples were obtained by means of an indwelling cardiac catheter before and 1, 3, 5, 10, 20, 30, and 60 min after suckling began. Measurements were performed at several stages of early, mid-, and late lactation. Oxytocin levels rose to peak values during suckling and declined rapidly after suckling stopped. PRL levels, on the other hand, did not reach peak values until 1-5 min after suckling had stopped, at which time plasma PRL concentrations plateaued and, in early and midlactation, were sustained at peak levels for 2-3 h; in late lactation, PRL secretion was not sustained after suckling had ceased. Peak PRL levels were relatively constant throughout most of lactation, with no significant differences between groups until late in lactation, when peak levels fell rather abruptly from a mean of 74 +/- 33.5 to 10.5 +/- 13.3 (+/- SD) ng/ml around day 25 in spite of a constant number of young and constant suckling frequency. Suckling failed to elicit any PRL release on day 30, but the administration of fluphenazine, a dopamine antagonist, did cause a rise in plasma PRL. Oxytocin release increased with advancing lactation, rising, on the average, 40 pg/ml on day 2 and to 250 and 490 pg/ml in mid- and late lactation, respectively. Dopaminergic agonist and antagonist drugs given to the doe before the nursing episode did not influence oxytocin release in response to suckling. Without a rise in plasma oxytocin, the young obtained no milk, but above a threshold level, there was no significant correlation between peak oxytocin levels and milk yield. When suckling failed to induce PRL secretion, milk secretion ceased rapidly in spite of copious oxytocin secretion. The failure of suckling to induce PRL release in late lactation, therefore, appears to be an important factor in the cessation of lactation.

Animals↗

Vasoactive intestinal peptide (VIP) stimulates oxytocin and vasopressin release from the neurohypophyis.

The concentration of vasoactive intestinal peptide (VIP) was measured by RIA in pituitary extracts of female cats; it was significantly higher in the posterior than in the anterior lobe, 47.3 +/- 3.9 pmol/g wet wt vs. 7.7 +/- 2.0 pmol/g wet wt (mean +/- SE, n = 5 in both instances). To investigate the effect of VIP on the release of posterior pituitary hormones, the concentration of arginine vasopressin and oxytocin was measured by RIA in jugular vein plasma during intracarotid infusion of VIP. The levels of both hormones rose during the 5-min infusion of VIP. Oxytocin levels increased from a mean of 7.9 microU/ml to a maximum of 34.9 microU/ml at 1 min and arginine vasopressin levels from from 27.4 microU/ml to a maximum of 157 microU/ml at 1 min. The levels of both hormones returned to baseline values in about 20 min. Since VIP has been localized to the nerve terminals of the neurohypophysis, these data suggest that endogenous VIP may play a role as a neurotransmitter in the magnocellular hypothalmo-neurosecretory system.

Animals↗

Oxytocin and initiation of human parturition. III. Plasma concentrations of oxytocin and 13,14-dihydro-15-keto-prostaglandin F2 alpha in spontaneous and oxytocin-induced labor at term.

The plasma concentrations of oxytocin and 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) were measured in serial samples collected during the first stage of spontaneous and oxytocin-induced labor in 17 and 15 women, respectively. Four women in late pregnancy served as control subjects, with serial samples collected at similar intervals as during labor. During spontaneous labor, mean plasma oxytocin levels were consistently raised over the levels observed 1 to 2 weeks before the onset of labor and were higher than the levels in the control patients (mean, 19.9 +/- 3.1 pg/ml) and the initial levels in the oxytocin-induced group of women (mean, 17.4 +/- 4.8 pg/ml). The mean plasma oxytocin levels during spontaneous labor (45 +/- 3.9 pg/ml) were similar to those observed during infusion of 4 to 6 mU/min of synthetic oxytocin (49.1 +/- 10.9 pg/ml). Plasma oxytocin levels increased progressively with stepwise increments of the infusion. Plasma PGFM levels also rose during labor, but, in contrast to the oxytocin levels which increased in early labor, plasma PGFM levels did not increase significantly until relatively late in labor, provided the membranes were intact. The state of the membranes had a marked influence on plasma PGFM; patients with spontaneous rupture of membranes had significantly increased PGFM levels when admitted early in labor or when membranes ruptured during labor. This increase in prostaglandin F2 alpha (PGF2 alpha) production does not by itself suffice to initiate labor, as evidenced by the failure of premature rupture of the membranes to initiate labor in a number of patients with elevated PGFM levels in whom labor was then induced with oxytocin. Conversely, oxytocin induction was successful only when PGFM levels increased during the infusion of oxytocin; in the absence of a rise in plasma PGFM, oxytocin induction failed. These data add support to the view that both oxytocin and PGF2 alpha are required for adequate stimulation of the human uterus during labor. In addition, the data suggest that oxytocin rather than PGF2 alpha may be the major stimulus that initiates labor, whereas PGF2 alpha appears responsible for the progress of labor.

Cervix Uteri↗

Oxytocin and the initiation of human parturition. IV. Plasma concentrations of oxytocin and 13,14-dihydro-15-keto-prostaglandin F2 alpha during induction of labor by artificial rupture of the membranes.

The influence of artificial rupture of the membranes on plasma levels of 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) and oxytocin was examined in 23 pregnant women at term. Serial blood samples were collected before and 15 minutes, 2 hours, 5 hours, and 8 hours after artificial rupture of the membranes. A significant rise in the concentration of plasma PGFM was observed at 15 minutes in the majority of women (20 of 23), but the magnitude of this early rise or the lack thereof was not related to the subsequent course of labor. The concentration of plasma PGFM at 2 hours was, on the other hand, significantly correlated with the induction-delivery interval. Amniotomy, by itself, induced labor and delivery when the increased PGFM levels were maintained from 2 to 5 hours after the procedure (n = 16). In those cases where Pitocin stimulation was required for adequate uterine contractions, it was found that plasma PGFM levels had declined to initial values at 2 hours. Pitocin infusions then partially reversed this decline. In one patient, the cervix failed to dilate in spite of prolonged Pitocin infusion which did not induce significant uterine contractions, and the infusion did not reverse the marked fall in plasma PGFM after the early but transient rise. Mean plasma oxytocin levels did not rise significantly during labor induced by artificial rupture of the membranes and were, on the average, similar to the levels observed during the first stage of spontaneous or oxytocin-induced labor. Considering the previously demonstrated maximal levels of uterine oxytocin receptors in early labor, the absence of a rise in the plasma oxytocin levels does not negate a role for oxytocin in working synergistically with prostaglandins in the mechanism of labor.

Amnion↗

[Effect of ritodrine on prostaglandin production in vivo and in vitro].

In 11 women between the 26th and 36th week of gestation the concentration of 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) was measured serially in the peripheral maternal plasma before and during treatment with ritodrine at a concentration of up to 350 mcg/min. On admission the mean plasma PGFM concentration was 268.0 +/- 43.3 pg/ml, which was significantly higher than the mean PGFM plasma level of the control group (156.0 +/- 21.8; n = 10). Treatment with ritodrine was successful in 7 women and led to a small, but statistically significant decrease in maternal plasma PGFM levels. In unsuccessful treated cases plasma PGFM levels also dropped initially, but increased again at 12 and 24 hours after initiation of therapy. The addition of ritodrine in concentrations of 10(-8) to 10(-6)M to the incubation medium led to a decrease in prostaglandin-(PG-)synthesis in vitro in the decidua and amnion. These changes were, however, only significant for PGE at a concentration of 10(-6)M in decidua and for PGE and PGF in a concentration of 10(-7)M in amnion. In the myometrium no effect of ritodrine on prostaglandin production could be observed. The measurement of PGFM production in the incubation vials indicated that ritodrine has no influence on the conversion of PGF2 alpha to its metabolite in any of these tissues. The results of the present study allow the following conclusions. 1. PGF2 alpha seems to play a role in the mechanism of premature labor. 2. In premature labor patients successful treated with ritodrine a significant decrease in circulating plasma PGFM levels is observed. In vitro ritodrine led to a small, but significant decrease in PGE and PGF synthesis in decidua and amnion which may add to the uterus-relaxing effect of ritodrine.

Amnion↗

[Oxytocin- and prostaglandin plasma concentrations before and after spontaneous labor: evidence of involvement of prostaglandins in the mechanism of placental separation].

The concentrations of oxytocin and PGE, PGF, and 13,14-dihydro-15-keto-PGF2 alpha (PGFM) in maternal peripheral plasma were measured in serial samples taken at full cervical dilatation and 5, 30 and 120 minutes postpartum. The prostanoid levels were also measured in serial samples of umbilical cord blood taken from the placental end in 4 instances. At full dilatation, plasma PGFM, but not PGE and PGF, was significantly raised over control (no labor) values. Just before or at the time of placental separation (5 minutes postpartum), the concentrations of PGF and PGFM were maximal, about twice the level at full dilatation. The level then decreased but at a slower rate than the metabolic clearance rates, indicating that considerable PGF production occurs in decidua and myometrium in the early postpartum period, after fetus, placenta, and the membranes are expelled. The rapid increase in the prostanoid concentrations in the umbilical cord blood draining the placenta after delivery of the infant suggests that the surge of prostaglandins 5 minutes postpartum originates in the placenta, and probably contributes to uterine contraction and placental separation and expulsion. Plasma OT was significantly raised over prelabor values at full cervical dilatation, and during the third stage, but dropped to control levels 30 minutes postpartum. Exogenous oxytocin infusions begun at delivery of the infant caused a marked increase in plasma OT and maintained the PGFM concentrations at a higher level than in the parturients not receiving oxytocin 2 hours postpartum.

Adult↗

Stimulation of myometrial and decidual prostaglandin production by amniotic fluid from term, but not midtrimester pregnancies.

The effect of amniotic fluid obtained from second trimester (16-20 wks) and term pregnancies (38-41 wks) on the production of PGE and F by human amnion, decidua and myometrium at term was determined using tissue slices incubated in vitro. Midpregnancy amniotic fluid neither inhibited nor stimulated the prostanoid production by any of the tissues. In contrast, term amniotic fluid obtained before as well as after the onset of labor markedly increased the production of both PGE and PGF in decidua and myometrium from levels in Krebs solution. The prostanoid production (PGE + PGF) in amnion was not significantly increased but the proportion of PGF was raised during incubations in term amniotic fluid. In decidua and myometrium the increase in PGE and PGF production in term amniotic fluid was approximately 200 and 400 percent respectively, from control values in Krebs solution. We propose that the stimulatory activity in term amniotic fluid is responsible for the accelerated synthesis of prostaglandins after rupture of membranes, which is reflected in raised PGF metabolite levels in maternal circulation. It may also be the reason for the rise in amniotic fluid prostaglandin levels around the 35th week of gestation, and perhaps for the onset of labor.

Amnion↗

Cervical ripening with intracervical prostaglandin-E2 gel. I. Clinical results and effect on plasma levels of oxytocin and 13,14-dihydro,15-ketoprostaglandin-F2 alpha.

Tylose gel containing 400 micrograms prostaglandin E2 in 3 ml gel was injected into the cervical canal of 20 patients with high-risk pregnancy and indication for induction of labor, but with unfavorable cervix. Ten were studied after the first gel application, five during repeat injection, and five after application of gel without PGE2. Blood samples were drawn serially during the first 8 hours for determination of oxytocin and 13,14-dihydro,15-ketoprostaglandin-F2 alpha (PGFM). The PGE2 gel increased the Bishop score within 8 hours in all patients; in half of them, artificial rupture of the membranes could be performed and labor induced without further gel application; in the others, it was repeated every 8 hours until a Bishop score of greater than or equal to 8 was achieved. Fourteen of the 15 PGE2-induced patients delivered vaginally. Mean PGFM levels did not increase significantly during the 8 hours of observation, but in patients who responded with rapid progression, an increase was seen after cervical dilation was 6 cm or more. The mean oxytocin levels increased within 60 minutes after PGE2 application and were increased for the remaining observation period. Application of inactive gel had no effect on cervical ripening nor on oxytocin or PGFM levels.

Adult↗

[Importance of oxytocin sensitivity for the spontaneous onset of human labor].

The significance of oxytocin for the onset of labour in humans is disputed, mainly because there is no increase in oxytocin concentration in the peripheral maternal blood before onset of labour. However, Fuchs et al. have recently shown that the concentration of oxytocin receptors in the myometrium is significantly higher directly before onset of labour than at the onset of spontaneous contractions. To establish a correlation with the clinical sensitivity to oxytocin, the authors determined the oxytocin sensitivity by means of intravenous administration of 3 X 10 m I.U. of oxytocin with continuous tocographic recording. Parallel to this determination, the cervical score was measured according to Bishop. The patients were 26 healthy pregnant women in whom both parameters were determined daily until onset of spontaneous labour pains. The sensitivity to oxytocin increased significantly during the last few days before spontaneous onset of labour. On the day before onset of pains, almost all of the pregnant women showed maximum sensitivity to oxytocin. Parallel to this, the cervical, scores also increased; on the day before onset of labour pains, almost all pregnant women had a cervical score of 5 or more than 5. On the basis of these results, which concur accurately with the results of measurement of oxytocin receptor concentrations, it is definitely possible to refute the arguments that oxytocin is irrelevant for the onset of labour because its concentration in the maternal plasma does not increase before the pains begin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

[Oxytocin (OT) and 13,14-dihydro-15-keto-PGF2 alpha (PGFM) levels after intracervical administration of PGE2 gel combined with administration of beta mimetics; biochemical changes and clinical consequences].

Intracervical application of 0.4 mg PGE2 gel for achieving maturity of the cervix before necessary inducement of labour results in 1-2% of the cases in permanent contractions in association with foetal bradycardias (Goeschen and Saling, 6). This Complication can be removed by the administration of the beta-mimetic Fenoterol given by the intravenous route. Basing on this fact we tried to find out whether it would be possible to prevent an increase in labour activity by administering Fenoterol before applying PGE2 without impairing the softening effect, and also how the OT and PGFM concentrations in the plasma are affected. To clarify this, we compared the clinical and biochemical results obtained in 5 patients who had been given 5 mg Fenoterol orally before receiving 0.4 mg PGE2 gel, with the results obtained in patients who had been treated without any previous Fenoterol administration with either 0.4 mg PGE2 (n = 10), 0.8 mg PGE2 (n = 6) or placebo gel (n = 5). In all groups treated with the preparation were obtained significant differences compared with the placebo group in respect of maturation of the cervix. Oral administration of Fenoterol did not produce any weaking of the softening effect; an increase of the dose to 0.8 mg did not result in an enhancement. After intracervical administration of 0.4 mg PGE2 gel the PGFM values remained unchanged with and without Fenoterol administration; the same was true also after 0.8 mg PGE2 and after placebo. As with spontaneous labour, a significant PGFM increase was seen only if the cervical diameter had attained 7 cm or more.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Topical↗

Effect of cervical application of prostaglandin (PG) E2 on plasma 13,14-dihydro-15-keto-PGF2 alpha and oxytocin in pregnant women at term.

The concentrations of 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) and oxytocin were measured by radioimmunoassay in the peripheral plasma of 21 women with low Bishop scores in whom cervical ripening and labour were induced with a cervical cap containing 1.5 mg of prostaglandin (PG) E2, left in place for 6 h. Blood samples were taken before and at 3, 6, 9 and 24 h after the cap was applied. Four women (control group) had a cap without PGE2. Labour began in 13 women receiving PGE2, 12 of whom were delivered within 24 h. In these women plasma PGFM rose progressively to levels seen during spontaneous labour, paralleling the changes in cervical dilatation. The increase became significant at 6 h, when cervical dilatation was 4.5 cm (SEM 0.5). Plasma oxytocin also increased significantly while the cap was in place and then decreased. Plasma PGFM and oxytocin did not change in the control subjects, and in the eight women needing further induction of labour the initial rises were transient and not statistically significant.

Cervix Uteri↗

Systemic and local regulation of oxytocin receptors in the rat uterus, and their functional significance.

Rats were made unilaterally pregnant by tying the right oviduct on the day after mating, to compare the oxytocin receptor concentrations in a nondistended, nonpregnant uterine horn with those in a distended, pregnant horn. On day 20, they were subjected to bilateral ovariectomy and indwelling balloons were inserted into both uterine horns. Following ovariectomy, the rats were injected im with either oil, estradiol benzoate (5 micrograms/rat per 24 h), or estradiol and progesterone together. For comparison, intact rats were studied on days 21 and 22, 24 and 48 h after insertion of the indwelling balloons. Spontaneous uterine activity and the response to increasing amounts of oxytocin were recorded 20-24 h and 44-48 h after surgery, following which the uteri were excised and assayed for oxytocin and estrogen receptors. The oxytocin receptor concentrations in the two horns were different on day 20 before the treatments were begun, the distended pregnant horn having a higher concentration per milligram DNA than the nonpregnant horn. The various treatments always changed the oxytocin receptor concentrations in the same direction; estrogen increased and progesterone inhibited the estrogen-induced rise in oxytocin receptor concentrations. In intact rats, the distention-induced increase in oxytocin receptor concentrations present on day 20 disappeared near term, but in the absence of the ovaries distention of the uterus had a significant influence on the myometrial oxytocin receptor concentrations, potentiating the effect of estrogen. Progesterone selectively inhibited the distention-induced increase in oxytocin receptor concentrations without inhibiting the hypertrophic effect of distention in general. A good correlation between oxytocin receptor numbers and tissue responsiveness was observed in all instances. The changes in spontaneous activity induced by the various treatments were distinct from the changes in oxytocin responsiveness. Estrogen exerted a strong inhibitory action on the activity stimulated by hormone withdrawal, while progesterone had no inhibitory effect. The pregnant distended horn always showed more spontaneous activity than the nonpregnant horn. There was an overall significant correlation between nuclear estrogen receptor and oxytocin receptor concentrations per milligram DNA, although the partial correlations were not significant in all groups (oil and progesterone).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Correlation between oxytocin receptor concentration and responsiveness to oxytocin in pregnant rat myometrium: effects of ovarian steroids.

Marked changes in the uterine binding of oxytocin (OT) occur in rats at the time of parturition or after treatment of ovariectomized rats with estrogen or progesterone. To ascertain that these binding sites represent the biological receptors for OT, we measured the uterine response to OT in various groups of rats in which specific OT binding was also determined. Intact pregnant rats and rats ovariectomized on day 20 of gestation and treated thereafter with oil, estradiol benzoate (5 micrograms/24 h), progesterone (5 mg/24 h), or estradiol and progesterone together had indwelling balloons inserted on day 20 for the recording of uterine response to either iv bolus injections or iv infusions of OT. The uterus was removed 24-48 h after balloon insertion, and OT binding to the particulate fraction as well as nuclear estrogen and cytosolic estrogen receptor concentrations were determined. An inverse correlation (r2 = 0.758) was found between the concentration of OT-binding sites and the threshold dose of OT, and a linear correlation was found between the concentration of binding sites and the uterine activity induced by OT infusion (r2 = 0.852). We conclude, therefore, that the high affinity (Kd, 1-2 nM) binding sites for OT represent the physiological receptors. The concentration of these sites increased progressively during estrogen treatment. Progesterone completely inhibited this estrogen-induced rise. After ovariectomy, there was a modest, but significant, increase in OT receptor concentration which also was prevented by progesterone. The increase in OT receptor concentration was correlated with the estrogen receptor concentration in intact pregnant and estrogen-treated ovariectomized animals, but not in the other groups of animals. The apparent affinity of the receptors for OT was not significantly affected by hormone treatment. We conclude that the concentration of receptors is a major factor controlling the uterine responsiveness to OT, and that the receptor concentrations are regulated by ovarian hormones in a manner related to estrogen receptor activation. In addition, estrogen appeared to enhance the coupling of OT receptor occupancy to the tissue response to OT.

Animals↗

Plasma levels of oxytocin and 13, 14-dihydro-15-keto prostaglandin F2 alpha in preterm labor and the effect of ethanol and ritodrine.

We have measured the concentrations of circulating oxytocin and the 13, 14-dihydro, 15-keto-metabolite of prostaglandin F2 alpha (PGFM) in women during preterm labor. Twelve women were given intravenous ethanol and 11 women received intravenous ritodrine for the prevention of preterm birth. Blood samples were obtained before and 1/2, 1, 2, 4, 12, and/or 24 hours after treatment began. On admission, the plasma concentrations of both oxytocin and PGFM were raised over levels observed in women with normal pregnancies of similar gestational age, 25 to 36 weeks. The initial oxytocin level was 58.5 +/- 8.2 pg/ml (mean +/- SE, n = 23) and the mean initial PGFM level was 264 +/ 33.1 pg/ml (n = 15); both values were significantly higher than in 10 control subjects (17.4 +/- 4.8 and 156 +/- 21.8 pg/ml, respectively). During infusion of ethanol, the plasma oxytocin level fell rapidly, the levels at 1/2 and 1 hour after infusion being significantly lower than before the infusion (29.0 +/- 5.5 and 27.8 +/- 3.5 pg/ml, respectively). The plasma oxytocin level remained low in women in whom the treatment arrested labor and prevented preterm birth (n = 8) but rose 2 to 4 hours after the infusion began in women in whom the treatment failed to arrest labor (n = 4). Ritodrine, on the other hand, had no significant effect on circulating oxytocin levels. The plasma PGFM level decreased significantly during ritodrine treatment only in the successfully treated patients. Ethanol had no consistent effect on plasma PGFM levels in the four patients in whom PGFM levels were measured. In the ritodrine-treated patients, the plasma PGFM level was positively correlated with the frequency of uterine contractions whereas in the ethanol-treated patients a correlation of plasma oxytocin to the frequency of contractions was observed. Thus, oxytocin secretion is increased during preterm labor, and the release of prostaglandin F is also increased. While it is not possible to determine whether any or both of these oxytocic agents actually trigger preterm labor, both seem to play a role in its mechanism.

Dinoprost↗

Oxytocin receptors and human parturition: a dual role for oxytocin in the initiation of labor.

The concentration of oxytocin receptors increased in the myometrium of pregnant women and reached maximum levels in early labor. Concentrations of oxytocin receptors were also high in the decidua and reached a maximum at parturition. In vitro, prostaglandin production by the decidua, but not by the myometrium, was increased by the addition of oxytocin. Oxytocin may therefore stimulate uterine contractions by acting both directly on the myometrium and indirectly on decidual prostaglandin production. Oxytocin receptors are probably crucial for the onset of human labor, and the stimulus for the increase in uterine prostaglandins may be oxytocin originating from the fetus.

Decidua↗

The origin of circulating 13,14-dihydro-15-keto-prostaglandin F2 alpha during delivery.

All uterine tissues as well as the fetal membranes and the placenta can form prostaglandins from endogenous precursors in vitro but it is not clear which of the tissues is the main site for the increase in PGF2 alpha production during human parturition. To examine this question, we measured plasma prostaglandin levels before and at intervals after expulsion of the fetus, placenta, and membranes. The concentration of PGFM at the beginning of the second stage of labor was significantly higher than before the onset of labor. Five minutes after the birth of the infant, the concentration had doubled. Thirty minutes after the expulsion of placenta and membranes, plasma PGFM had fallen to the levels at full dilatation; two hours postpartum it was still significantly raised over levels before labor. Since the halflife of PGFM in the circulation is about 7 minutes, these findings indicate that the uterine tissues are important sources of PGFM during labor. In contrast, endogenous oxytocin levels, which were significantly raised over control levels at the second stage of labor, did not change during the third stage, and declined postpartum to control levels. Oxytocin infusion did not influence PGFM levels at 5 and at 30 minutes postpartum, but raised them at 2 hours.

Adult↗

[Does fetal oxytocin initiate human labour? A hypothesis].

The concentration of specific oxytocin receptors increases during pregnancy and reaches a maximum at term after the onset of spontaneous labour. This constitutes a biochemical explanation for the well-known increase of oxytocin sensitivity during pregnancy. Oxytocin receptors were also found in human decidua and their concentration increased similarly. Based on these results the hypothesis was set up that oxytocin leads to an increase in prostaglandin production though specific receptors in decidua. Under specific incubation circumstances oxytocin indeed increased prostaglandin E and prostaglandin F synthesis of decidual tissue. In induction of labour with oxytocin PGF-levels in the maternal peripheral plasma increased significantly in all women in whom induction was successful. Since it is known that the fetus secretes considerable amounts of oxytocin in case of labour of spontaneous onset the hypothesis was set up that fetal oxytocin may initiate human labour by the mechanisms described above.

Decidua↗