Influence of linoleic/linolenic acid ratio in the diet of periparturient cattle on plasma concentrations of PGF2 alpha metabolite and placental expulsion rate

Forty-eight cows Holstein Friesian x Dutch Friesian (HF x DF) were randomly assigned to 2 groups fed 1 of 2 diets (isocaloric and isonitrogenous but different in linoleic/linolenic acid ratio) from 4 wk before expected parturition until 7 d after calving. Effects of the diet on plasma linoleic/linolenic acid ratio, plasma PGFM levels and placental explusion rate were studied. Dietary treatment resulted in significant differences in linoleic/linolenic acid ratio in blood plasma (1.00 +/- .22 vs 4.41 +/- .53). The placental expulsion rate was not significantly different between the 2 treatment groups. Plasma PGFM levels, as analyzed for 28 cows from 30 d before parturition until 1.5 d after parturition, were similar for the diets. Cows with a longer placental expulsion rate had lower PGFM levels at parturition (for instance, placental expulsion rate shorter (n = 11) and longer (n = 17) than 6 h, 1248 vs 2965 pg/ml, residual standard deviation 1185 pg/ml, P < 0.01). The results show that the dietary linoleic/linolenic acid ratio can influence the plasma linoleic/linolenic acid ratio without affecting the placental expulsion rate or plasma PGFM levels around parturition.     

Incidence of retained placenta following induction of parturition with corticoids or prostaglandins

Three trials involving 214 cows were conducted to 1) compare the timing of events during normal parturition with parturition induced with a corticoid or a prostaglandin; 2) determine if synchrony could be improved by injection of steroids either concurrently or after injection of a corticoid or a prostaglandin; 3) determine if the incidence of retained placenta could be reduced; and 4) explore methods of treating retained placenta. The timing of events following induction of parturition was compared with that following a normal parturition in 76 heifers. The time from onset of labor to appearance of the placenta, abdominal press, appearance of feet and expulsion of the fetus did not differ between normal and induced parturition. The time from onset of labor to calf standing was increased from 2.3 +/- 2.0 hours in normal parturition to 5.8 +/- 5.5 hours in cows receiving 10 mg of flumethazone (P<0.05). The interval from onset of labor to calf nursing also tended to be longer (P>0.05<0.01). All control cows expelled fetal membranes by 48 hours after onset of labor, but the proportion expelled by the treatment groups varied from 24 to 76%. None of the treatments used in this study significantly increased placental expulsion over that noted when flumethazone or prostaglandins were used alone. No difference in placental expulsion time was noted in cows douched with nolvasan or injected with 30 cc oxytetracycline. None of the treatments used in the three trials reported in this study improved synchrony of parturition over that noted in the cows receiving only an injection of flumethazone or prostaglandins.     

The relationship between plasma oestrone sulphate concentrations in pregnant dairy cattle and calf birth weight, calf viability, placental weight and placental expulsion

A total of 54 Holstein-Friesian cows (13 primiparous and 41 multiparous) was used to study maternal plasma oestrone sulphate (E1S) during pregnancy and its relationship to birth weight and viability of calves and time required for placental expulsion after calving. Plasma samples were obtained from the tail vein of cows once every month from days 90 to 180, every 2 weeks from days 181 to 270, and every day from day 270 of gestation to parturition. The E1S concentrations were measured by radioimmunoassay, and birth weight, placental measurements, neonatal viability and the period from calving to placental expulsion were recorded. E1S concentrations were correlated positively (0.71 > or = r > or = 0.32, P < 0.05 or P < 0.01) with calf birth weight and weights of cotyledons, intercotyledonary membranes and total placenta from days 210 of gestation to 1 day prepartum. Calf birth weight was correlated positively (p < 0.01) with the weight of the cotyledons (r = 0.87), intercotyledonary membranes (r = 0.78) and total placenta (r = 0.88). In addition, E1S concentrations were positively correlated (0.63 > or = r > or = 0.28, P < 0.05 or P < 0.01) with the neonatal viability after day 195 of pregnancy, and were negatively correlated (-0.29 > or = r > or = -0.55, P < 0.05 or P < 0.01) with the intervals from parturition to placental expulsion after 225 days of pregnancy. The results suggest that variation among dams for circulating E1S levels during late pregnancy may be caused by variation of placental development and ability for oestrogen production and conjugation, and they may influence fetal growth, neonatal viability and retained placenta.     

Pre-parturition profile of steroids and prostaglandin in cows with or without foetal membrane retention

Retained foetal membranes in cattle is one of the most common complications associated to the reduction in milk yield and impaired fertility in dairy cattle. In order to determine some endocrine mechanisms controlling parturition and delivery of foetal membranes, plasma concentrations of steroids and prostanoids were determined in 20 healthy Holstein cows. Samples were taken within the interval of 5 days pre-parturition to 12h after calving. Progesterone (P4) levels were similar in cows with (PR) and without (NPR) placental retention. While the estradiol-17beta (E2) peak at parturition was lower in PR than in NPR cows, cortisol levels were greater in PR cows 12 and 24h pre-parturition. The Prostaglandin F2alpha metabolite (PGFM) levels were higher at parturition in NPR compared with the PR group, but 12h later, these levels in the PR group increased so that concentrations were greater as compared with NPR cows. The Prostaglandin E2 metabolite (PGEM), 24, 48 and 72 h pre-parturition, were higher in PR cows. However, the PGFM:PGEM ratio was greater in cows up NPR at all time when included, indicating the importance of higher levels of Prostaglandin F2alpha (PGF2alpha) than Prostaglandin E2 (PGE2) for normal placental delivery. In conclusion, placental retention was related to both estrogen and PGF2alpha deficiency, which may be a consequence of metabolic stress leading to PGE2 and maternal cortisol synthesis before parturition.     

The role of endogenous estrogens in the maturation process of the bovine placenta

The plasma estrogen and progesterone concentrations of 19 pregnant cows (average duration of pregnancy 266.0 +/- 2.3 d at the start of the study) were determined daily from Day 6 pre partum to Day 1 post partum. Parturition was induced in all cows by administration of 10 mg i.m. flumethasone. Values were centered around the delivery date (Day 0) following either induced normal calving (n = 3) or surgical delivery (n = 16). In animals showing spontaneous expulsion of the fetal membranes (Group 1, n = 6) the average total estrogen concentration increased significantly from Day 6 until Day 1 before parturition (1329.2 +/- 317.9 to 3719.8 +/- 951.2 pg/ml in total estrogens). A marked decrease was observed on Day 1 post partum (459.4 +/- 344.2 pg/ml). In comparison with Group 1, animals showing either a delayed or partial expulsion of the fetal membranes, or in which the placenta could be withdrawn 16 h after calving (Group 2, n = 5), had consistently lower total estrogen concentrations between Day 6 (595.4 +/- 174.8 pg/ml) and Day 1 (1884.3 +/- 565.1 pg/ml) before parturition. The estrogen values of the cows with retained placenta (Group 3, n = 8) from Days 6 to 0 pre partum were significantly lower than those of Group 2. Total estrogen concentrations of the three groups 1 d post partum did not differ significantly. It is generally recognized that estrogens play an important role in the maturation process of the placentomes. Our investigation demonstrates that not only is the magnitude of the prepartum rise in estrogens of great influence of the maturation process but the duration of this rise is likewise important. These two factors are vital for a normal expulsion of the fetal membranes.     

Ultrastructural changes in the placenta of the ewe following foetal infusion of cortisol.

The placental changes which followed continuous infusion of cortisol into the sheep foetus in the later stages of gestation were, like the hormonal changes, broadly similar to those of spontaneous parturition. There was, however, a premature separation of foetal and maternal tissues in certain areas of the placental cotyledons, and this separation appeared to protect the foetal epithelium from the degenerative changes which normally take place in the short space of time between the birth of the lamb and the delivery of the foetal membranes. The results suggest that an experimental model in which premature labour is induced by the administration of cortisol to the foetus is probably incomplete, and that additional factors almost certainly contribute to the cascade phenomenon of spontaneous parturition.     

Lambing and placental expulsion time after dexamethasone-induced parturition in Corriedale and Polwarth ewes

To study breed differences in ewes induced to parturition with dexamethasone (DXM), 15 Corriedale and 16 Polwarth ewes were injected with 15 mg of DXM four days before the expected lambing date (Days 144 and 145, respectively) in Experiment 1. Interval from treatment to parturition was twice as long for the Polwarth than for the Corriedale breed (57.9 vs 28.8 hours, P /= 0.05) and on the percentage of ewes retaining the placenta beyond 6 hours (18% vs 0%, P>/= 0.05). Birth weight of lambs was lower in the induced group (3.9 vs 4.5 kg, P相似文献   

Prolongation of parturition in the pregnant rat following treatment with a platelet activating factor receptor antagonist

The presence of platelet activating factor (PAF) in amniotic fluid of women only in labor is indicative of a role for PAF in parturition. In addition, stimulated amnion membrane produces both PAF and prostaglandin E2, each of which is capable of inducing myometrial contraction. To evaluate the involvement of PAF in the process of parturition, we administered the PAF receptor antagonist, L-659,989, to 17-day timed pregnant rats and followed the events of labor and delivery. Administration by mouth with L-659,989 of three concentrations (1.6, 16, and 48 mg/kg/day) did not alter the gestational period; however, the duration of parturition was increased from 2-fold to 5-fold by such treatment. No toxicity of the analog was apparent; treated dams showed no signs of morbidity, and fetal mortality was not significantly altered by treatment with the antagonist. Based on these experiments, it is suggested that the PAF receptor antagonist interferes with the normal progression of events of parturition and that PAF is an integral mediator in initiating the myometrial contraction necessary for expulsion of the fetus.     

Arachidonic acid metabolism by bovine placental tissue during the last month of pregnancy

Conversion of tritiated arachidonic acid (AA) into metabolites of the cyclo- and lipoxygenase pathways by bovine fetal placental tissue (200 mg) and fetal plus maternal placental tissue (400 mg) of Days 255, 265, 275 of gestation and at parturition (n = 5) during a 30 min incubation was measured using reverse-phase high pressure liquid chromatography. Fetal placental tissue produced 13,14-dihydro-15-keto-prostaglandin E2 (PGEM) as the major metabolite, the synthesis of which increased from Day 265 to Day 275 and parturition by 150% and 475%, respectively. In tissues collected at parturition, PGE2 synthesis was also detected. On Day 275 and at parturition fetal placental tissue synthesized the metabolite 12-hydroxyheptadecatrienoic acid (HHT), and throughout the experimental period the lipoxygenase product 15-HETE was detected with synthesis rates increasing over time of gestation. In addition, an unidentified metabolite was regularly found in the radiochromatograms which eluted at 1 h and 1 min (U101), between HHT and 15-HETE. The synthesis of this metabolite decreased as pregnancy progressed. Furthermore, various other polar and nonpolar metabolites pooled under the heading UNID were eluted, the production of which increased over time of gestation. The presence of maternal placental tissue did not influence the synthesis of PGEM, 15-HETE and U101, but the production of HHT was decreased when maternal tissue was present. Also, as pregnancy progressed, maternal placental tissue seemed to contribute to the pool of unidentified metabolites. In conclusion, fetal placental tissue seems to be the major source of the AA metabolites when compared with maternal placental tissue, and AA metabolism by bovine placental tissue is markedly increased throughout the last month of pregnancy, suggesting a role for AA metabolites in mechanisms controlling parturition.     

Parturition in gilts: duration of farrowing, birth intervals and placenta expulsion in relation to maternal, piglet and placental traits

Large White x Meishan F2 crossbred gilts (n = 57) were observed continuously during farrowing while the placentae of their offspring were labeled in order to examine the duration of farrowing and placenta expulsion in relation to maternal-, piglet- and placental traits and the duration of birth interval in relation to birth weight, birth order and placental traits. Independently from each other, litter size, gestation length and offspring directed aggression significantly (P 0.05) affected duration of farrowing. An increase in litter size was associated with an increase of duration of farrowing and an increase in gestation length was associated with a decrease of duration of farrowing. Aggressive gilts took longer to farrow, compared to non-aggressive ones. After taking into account litter size, gestation length and offspring directed aggression, placental thickness (i.e., placental weight corrected for placental surface area) was significantly (P < 0.05) related to duration of farrowing, i.e., litters with on average thicker placentae took longer to farrow. The latter effect is the result of the fact that individual placental thickness significantly (P < 0.01) affected individual birth interval, independent of birth weight. The piglet has to break its own membranes to be able to start its journey through the uterus towards the birth channel. Apparently, a thicker placenta offers more resistance and thus prolongs the process of birth. Independent of placental thickness, birth interval significantly (P < 0.01) decreased with an increase in birth order (first born to last born). The high variation of birth intervals for the last born piglets, caused a slight increase in average birth interval for the latter piglets. Litters with on average more areolae per placenta took significantly (P < 0.001) less time to be born than litters with on average less areolae per placenta (independent of total number of piglets born and other placental traits), while birth intervals within litters were not affected by this trait. Thus, these results are probably due to a gilt trait rather than a piglet trait. Since the number of areolae represent the number of uterine glands present, the gilt trait might be uterine development. Duration of placenta expulsion significantly (P < 0.01) increased with an increase of duration of farrowing. Furthermore, the first placenta was expelled significantly (P < 0.01) earlier relative to last piglet when duration of farrowing was protracted, while there was no relation of the time interval between first placenta and last piglet and the duration of placenta expulsion. In conclusion, the most important finding of this study is that placental thickness rather than birth weight appears to play an important role in the duration of birth intervals and as a result, of duration of parturition in gilts.     

Apoptosis in human term placenta is not increased during labor but can be massively induced in vitro.

Apoptosis in human placental villi is reported to increase until close to delivery. However, the involvement of the apoptotic process in the initiation of labor, and more particularly in relation to the decrease in placental perfusion during uterine contractions, remains unknown. The purpose of the study was to examine the reactivity of the apoptotic machinery in term placentae obtained before or after the onset of labor and after in vitro incubations. The incidence of apoptotic nuclei (< 1%) as evidenced by the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) method, and the histological distribution of immunoreactive Bcl-2, Bax, and Bcl-x proteins, were similar in placentae collected after delivery and before the onset of labor and in placental explants maintained overnight at 4 degrees C in a minimal salt-Hepes medium. By contrast, 28% of nuclei contained fragmented DNA when placental explants were incubated overnight at 37 degrees C. This marked increase was associated with a decrease in the intensity of the Bcl-2 immunostaining and an increase in the intensity of Bax and Bcl-x immunostaining. In conclusion, the present study clearly evidences the presence of an active apoptotic machinery in term placental cells that is not involved in normal parturition.     

Matrix metalloproteinase-1 and -9 in human placenta during spontaneous vaginal delivery and caesarean sectioning in preterm pregnancy

Preterm birth is a major public health problem in terms of loss of life, long-term and short term disabilities worldwide. The process of parturition (both term and preterm) involves intensive remodelling of the extracellular matrix (ECM) in the placenta and fetal membranes by matrix metalloproteinases (MMPs). Our previous studies show reduced docosahexaenoic acid (DHA) in women delivering preterm. Further omega 3 fatty acids are reported to regulate MMP levels. This study was undertaken to examine the placental levels of MMPs and their association with placental DHA levels in women delivering preterm. The levels of MMP-1 and MMP-9 in 74 women delivering preterm (52 by spontaneous vaginal delivery and 22 by caesarean sectioning) and 75 women delivering at term (59 by spontaneous vaginal delivery and 16 by caesarean sectioning) were determined by enzyme-linked immunosorbent assay (ELISA) and their association with placental DHA was studied. Placental MMP-1 levels were higher (p<0.05) in women delivering preterm (both by spontaneous vaginal delivery and caesarean sectioning) as compared to those delivering at term. In contrast, placental MMP-9 levels in preterm pregnancies was higher (p<0.05) in women with spontaneous vaginal delivery while lower (p<0.05) in women delivering by caesarean sectioning. Low placental DHA was associated with higher placental MMP-9 levels. Our study suggests a differential effect of mode of delivery on the levels of MMPs from placenta. Further this study suggests a negative association of DHA and the levels of MMP-9 in human placenta although the mechanisms need further study.     

Adrenomedullin in perinatal medicine

This review will consider whether adrenomedullin (AM) plays a role in the different aspects of perinatal medicine: contributing to maternal systemic vasodilatation during pregnancy, regulating uterine and placental blood flow, being involved in the process of implantation and participating in uterine quiescence prior to parturition. In addition, this will also consider whether a modification of AM secretion contributes to some pathological conditions in pregnancy such as preeclampsia and impairment of fetal growth. The biosynthesis of AM increases in gravid rats and in pregnant women, and the placenta represents an important site of AM production during pregnancy. Both the peptide and its receptors have been found in the uterus, placenta, fetal membranes and cord vessels, and fetal membranes and placental tissues in culture secrete AM. AM contributes to maternal systemic vasodilatation, the placental vessels are relaxed by AM in a dose-dependent manner and AM is expressed in the fetoplacental and umbilical vascular endothelium where basal production of AM contributes to low fetoplacental vascular resistances. Controversy exists over the status of circulating and placental AM in preeclampsia and of the relative contribution of AM to impaired fetoplacental circulation and fetal growth. Moreover, the uterus expresses AM mRNA and exogenous AM relaxes the myometrium in a dose-dependent manner; however, clinical studies have shown that AM does not decrease before the onset of parturition. Rather, AM secretion increases during spontaneous labor and in preterm delivery.     

Questionnaire-based survey of parturition in the queen

The lack of scientific data concerning whether parturition in the queen proceeds normally or not may prevent veterinarians and cat owners from recognizing parturition problems in time. A questionnaire-based study of parturition in 197 queens was performed to determine several parameters of parturition and their influence on its progress. The mean length of gestation was 65.3 days (range 57 to 72 days) and it decreased with increasing litter size (P = 0.02). The median litter size was 4.5 kittens (range 1 to 9), with more males (53%) than females (46%) (P = 0.05). Sixty-nine percent of the kittens were born in anterior presentation and 31% in posterior presentation, indicating that either can be considered normal in the cat. Males were born in posterior position (34%) more often than females (26%) (P = 0.03). The mean birth weight was 98 g (range of 35 to 167 g) and decreased with increasing litter size (P < 0.01). Mean birth weight was higher in males and kittens born in posterior presentation (P < 0.01). Forty-four (5%) of the 887 kittens were stillborn. This was not correlated with the presentation at expulsion but stillborn kittens were more often female (P = 0.02) and weighed less than those born alive (P = 0.04). The median interkitten time was 30 min (range 2 to 343 min) and 95% were born within 100 min after expulsion of the preceding kitten. The interkitten time as a measure of the progress of parturition was not influenced by the kitten's gender, presentation at expulsion, birth weight, or stillbirth, or by the parity of the queen. The results of this study can be used to develop reference values for parturition parameters in the queen, both to determine whether a given parturition is abnormal and as the basis for a parturition protocol.     

Haemostatic Mechanism in the Uterine Circulation during Placental Separation

The haemostatic mechanism in the uterus during parturition was investigated in 12 patients being delivered by caesarean section. Detailed sequential study of the blood coagulation and fibrinolytic systems in the uterine circulation showed that placental separation is accompanied by a striking local activation of the clotting mechanism. Uterine vein blood draining the placental site while the placenta was separating showed a pronounced shortening of the whole-blood clotting-time, a significant shortening of other clotting-tests, and a sharp increase in factor VIII activity, though these changes were transitory. After delivery the level of fibrinogen and circulating platelets steadily increased and factor VIII activity remained high.Activation of the clotting mechanism during placental separation appears to play an essential part in controlling uterine haemorrhage. The subsequent changes in the haemostatic mechanism in the puerperium are likely to predispose to thromboembolic complications.     

Inhibition of progesterone secretion by a 3 beta-hydroxysteroid dehydrogenase inhibitor in late pregnant sheep

The role of progesterone in the initiation of parturition in the sheep is unclear. Whether a decrease in plasma progesterone is the essential prerequisite for the initiation of parturition or whether other factors also maintain uterine quiescence until delivery is not known. The effect of withdrawal of progesterone on the initiation of parturition has been investigated by intravenous administration of trilostane, a 3 beta-hydroxysteroid dehydrogenase delta 5-4 isomerase inhibitor, to late pregnant sheep. Twenty-five or 100 mg trilostane caused a precipitous decrease in plasma progesterone to about 30% of preinjection levels. Progesterone remained depressed for up to 7 days after treatment. 13,14-Dihydro-15-keto-prostaglandin F2 alpha (PGFM) became elevated between 7 and 36 h after trilostane injection but gradually returned to preinjection levels during the subsequent 36 h, at a time when plasma progesterone was still depressed. Four of 11 animals treated with 100 or 200 mg trilostane aborted prematurely at a time when plasma PGFM was maximal and plasma progesterone minimal. There were no consistent changes in plasma estradiol-17 beta or ovine placental lactogen concentrations after treatment with trilostane. It is suggested that a decrease in plasma progesterone will cause a transient increase in plasma PGFM concentrations which can lead to the premature initiation of parturition. In some instances the myometrium does not appear to respond to the elevated PGFM concentrations even when the estrogen:progesterone ratio is elevated by a decrease in plasma progesterone.     

NODAL in the uterus is necessary for proper placental development and maintenance of pregnancy

Preterm birth is the single leading cause of perinatal mortality in developed countries, affecting approximately 12% of pregnancies and accounting for 75% of neonatal loss in the United States. Despite the prevalence and severity of premature delivery, the causes and mechanisms that underlie spontaneous and idiopathic preterm birth remain unknown. Our inability to elucidate these fundamental causes has been attributed to a poor understanding of the signaling pathways associated with the premature induction of parturition and a lack of suitable animal models available for preterm birth research. In this study, we describe the generation and analysis of a novel conditional knockout of the transforming growth factor beta (TGFB) superfamily member, Nodal, from the maternal reproductive tract of mice. Strikingly, uterine Nodal knockout females exhibited a severe malformation of the maternal decidua basalis during placentation, leading to significant intrauterine growth restriction, and ultimately preterm birth and fetal loss on Day 17.5 of gestation. Using several approaches, we characterized aberrant placental development and demonstrated that reduced proliferation combined with increased apoptosis resulted in a diminished decidua basalis and compromised maternal-fetal interface. Last, we evaluated various components of the established parturition cascade and determined that preterm birth derived from the maternal Nodal knockout occurs prior to PTGS2 (COX-2) upregulation at the placental interface. Taken together, the results presented in this study highlight an in vivo role for maternal NODAL during placentation, present an interesting link between disrupted decidua basalis formation and premature parturition, and describe a potentially valuable model toward elucidating the complex processes that underlie preterm birth.     

Parturition in horses is dominated by parasympathetic activity of the autonomous nervous system

External and internal stressors prolong parturition in different species. At parturition, sympathoadrenal activation should be avoided because an increased sympathetic tone may cause uterine atonia via β₂-receptors. We hypothesized that at physiological parturition, horses are under parasympathetic dominance, and stress-response mechanisms are not activated during delivery of the foal. To evaluate stress responses, heart rate, heart rate variability, catecholamines, and cortisol were analyzed in mares (n = 17) throughout foaling. Heart rate decreased from 2 hours before (51 ± 1 beats/minute) to 2 hours after delivery (41 ± 2 beats/minute; P < 0.05). Heart rate variability variables, standard deviation of the beat-to-beat interval, and root mean square of successive beat-to-beat differences, changed over time (P < 0.05) with the highest values within 15 minutes after delivery. The number of mares with atrioventricular blocks and the number of atrioventricular blocks per mare increased over time (P < 0.01) and were significantly elevated from 15 minutes before to 45 minutes after birth of the foal. Salivary cortisol concentrations increased to a maximum at 30 minutes after delivery (25.0 ± 3.4 ng/mL; P < 0.01). Plasma epinephrine and norepinephrine concentrations showed significant fluctuations from rupture of the allantochorion to expulsion of the fetal membranes (P < 0.01) but were not markedly elevated at any time. In conclusion, mares give birth under high parasympathetic tone. Cortisol release during and after foaling is most likely part of the endocrine pathways regulating parturition and not a labor-associated stress response.     

Initiation of parturition in humans.

The mechanism by which parturition is initiated in humans is largely unknown. The placenta and fetal membranes appear to play the major role in the initiation of labour, and the fetus may influence the timing of labour. Clinical observations and experiments with animals have revealed that placental neuropeptides may be able to control steroid metabolism and trigger the onset of labour, while the fetus may be able to interact with such events to initiate parturition at an appropriate time. However, further study is needed to determine the role of placental releasing factors and glycoprotein hormones and their ability to control placental steroid metabolism.     

Glucocorticoid regulation of human and ovine parturition: the relationship between fetal hypothalamic-pituitary-adrenal axis activation and intrauterine prostaglandin production

Birth in many animal species and in humans is associated with activation of hypothalamic-pituitary-adrenal function in the fetus and the increased influence of glucocorticoids on trophoblast cells of the placenta and fetal membranes. We suggest that in ovine pregnancy glucocorticoids directly increase fetal placental prostaglandin production, and indirectly increase prostaglandin production by maternal uterine tissues through the stimulation of placental estradiol synthesis. The events of ovine parturition are compared with those of human parturition. In the latter, we suggest similar direct effects of glucocorticoids on prostaglandin synthesis and metabolism in fetal membranes and similar indirect effects mediated by glucocorticoid-stimulated increases in intrauterine corticotropin-releasing hormone expression.