Activin A, inhibin A, inhibin B and parturition: changes of maternal and cord serum levels according to the mode of delivery.

OBJECTIVE: To evaluate whether activin A, inhibin A, and inhibin B levels in maternal and umbilical artery serum change according to the mode of delivery. DESIGN: Maternal and cord blood specimens were collected at term after spontaneous labour and vaginal delivery, or elective caesarean section. SETTING: Universities of Pisa, Turin, Naples and Udine. POPULATION: Forty-two healthy pregnant women, at 3940 weeks of gestation, divided into two subgroups: group 1 vaginal delivery (n = 21), were delivered of 10 female and 11 male infants; group 2 elective caesarean section (n = 21), were delivered of 11 female and 10 male infants. MAIN OUTCOME MEASURES: Serum activin A, inhibin A, inhibin B concentrations in maternal and umbilical cord blood. RESULTS: At vaginal delivery, maternal serum inhibin A and inhibin B levels were lower and activin A levels higher than at elective caesarean section. Maternal levels of activin A, inhibin A and inhibin B were constantly higher than in umbilical arterial blood, independent of the mode of delivery. No significant difference was observed in umbilical arterial serum levels of the three proteins between the two modes of delivery. Umbilical arterial serum activin A and inhibin A concentrations did not show a significant difference between male and female infants in either vaginal or caesarean section, but male infants showed inhibin B levels significantly higher than female, independent of the mode of delivery. CONCLUSIONS: In the presence of active labour, the human placenta secretes larger amounts of activin A and lesser amounts of inhibin A and inhibin B into the maternal circulation. Inhibin-related proteins in the fetal circulation do not show differences according to the mode of delivery, suggesting that they have a different method of production or metabolic rate compared with maternal activin and inhibins.     

Activin A, inhibin A, inhibin B and parturition: changes of maternal and cord serum levels according to the mode of delivery

Objective To evaluate whether activin A, inhibin A, and inhibin B levels in maternal and umbilical artery serum change according to the mode of delivery.
Design Maternal and cord blood specimens were collected at term after spontaneous labour and vaginal delivery, or elective caesarean section.
Setting Universities of Pisa, Turin, Naples and Udine.
Population Forty–two healthy pregnant women, at 39–40 weeks of gestation, divided into two subgroups: group 1 vaginal delivery (   n = 21  ), were delivered of 10 female and 11 male infants; group 2 elective caesarean section (   n = 21  ), were delivered of 11 female and 10 male infants.
Main outcome measures Serum activin A, inhibin A, inhibin B concentrations in maternal and umbilical cord blood.
Results At vaginal delivery, maternal serum inhibin A and inhibin B levels were lower and activin A levels higher than at elective caesarean section. Maternal levels of activin A, inhibin A and inhibin B were constantly higher than in umbilical arterial blood, independent of the mode of delivery. No significant difference was observed in umbilical arterial serum levels of the three proteins between the two modes of delivery. Umbilical arterial serum activin A and inhibin A concentrations did not show a significant difference between male and female infants in either vaginal or caesarean section, but male infants showed inhibin B levels significantly higher than female, independent of the mode of delivery.
Conclusions In the presence of active labour, the human placenta secretes larger amounts of activin A and lesser amounts of inhibin A and inhibin B into the maternal circulation. Inhibin–related proteins in the fetal circulation do not show differences according to the mode of delivery, suggesting that they have a different method of production or metabolic rate compared with maternal activin and inhibins.     

Human corticotropin-releasing hormone during pregnancy

Elevated irCRH levels up to 14 ng/ml were measured in 176 females in the last trimester. The highest maternal CRH levels were found in those females in whom the period from the onset of labour to full dilatation of the cervix and the time span of delivery were shortest. irCRH in amniotic fluid (120 +/- 180 pg/ml; n = 14) was in the same range as in umbilical cord plasma (233 +/- 188 pg/ml; n = 66) and 20-fold lower than in prepartal maternal plasma (5.38 +/- 4.49 ng/ml; n = 66). irCRH in maternal plasma correlated highly to irCRH in umbilical cord plasma (p less than 0.001; n = 66). After delivery irCRH disappeared from maternal plasma with a half-life of 50 minutes (n = 14). One day postpartum irCRH levels (n = 22) were undetectable. The height of the irCRH levels in the various biological fluids did not correlate to the mode or the pathological events of delivery (n = 43). Maternal ACTH levels above the normal range were encountered only in women immediately prepartal and did not correlate to the CRH levels (253 +/- 229 pg/ml; n = 66). Cortisol levels were higher in maternal plasma than in umbilical cord plasma due to elevated CBG (n = 78). Free cortisol levels were higher in the 3rd trimester than in the 1st (2.18 +/- 0.16 vs 1.16 +/- 0.73 ng/ml; n = 42). irCRH in maternal and umbilical cord plasma correlated to the hPl and estriol levels (p less than 0.001 and p less than 0.05; n = 66). We conclude that irCRH is secreted by the placenta into both maternal and fetal circulation. Though placental CRH is undistinguishable from hypothalamic CRH, the biological significance of placental CRH remains open. Our data show that placental CRH might be responsible for the changed function of the adrenal gland during pregnancy, with higher free cortisol levels in the last trimester. The extremely elevated ACTH levels during labour and delivery indicate that CRH is not the only mediator of stress-induced ACTH secretion in the regulation of the maternal hypothalamo-pituitary-adrenal axis.     

Labour-associated expression of intercellular adhesion molecule-1 (ICAM-1) in placental endothelial cells indicates participation of immunological processes in parturition.

Inflammatory cytokines induce or upregulate de novo expression of cell adhesion molecules on endothelial and epithelial cells. In order to demonstrate inflammatory reactions within placental tissues in association with normal term as well as non-infection-induced preterm labour, the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and endothelial leucocyte adhesion molecule-1 (ELAM-1) was examined by immunohistochemical methods in both trophoblastic villi (n=123) and umbilical cord (n=61). As a result, ICAM-1 immunoreactivity was exclusively localized in the endothelial cells of the fetal vascular system, while VCAM-1 and ELAM-1 were not detected. Whereas ICAM-1 was not expressed in early pregnancy (9-12 weeks of gestation), it could be weakly detected at the end of pregnancy in cases of elective caesarean delivery in the absence of labour, and was significantly more strongly expressed in cases of vaginal delivery after spontaneous onset of normal term labour. Significantly increased immunoreactivity of ICAM-1 within umbilical cord tissues was also found in association with uncontrollable preterm labour in the absence of intrauterine infection which was excluded after histological examination of fetal membranes, umbilical cord and chorionic plate. We conclude that ICAM-1 expression in the endothelium of the fetal vascular system is associated with the presence of labour and reflects participation of immune-inflammatory reactions in labour-promoting mechanisms.     

The effect of labour and placental separation on the shedding of syncytiotrophoblast microparticles, cell-free DNA and mRNA in normal pregnancy and pre-eclampsia

The clinical features of the maternal syndrome of pre-eclampsia can be explained by generalised maternal endothelial cell dysfunction, which is a part of a more global maternal systemic inflammatory response. There is growing evidence that these effects are associated with the shedding of cellular debris, including syncytiotrophoblast microparticles (STBM), cell-free DNA and mRNA, from the surface of the placenta (syncytiotrophoblast) into the maternal circulation. The increased shedding of this debris seen in pre-eclampsia is believed to be caused by placental ischaemia, reperfusion and oxidative stress. This study was carried out to determine whether uterine contractions during labour and subsequent placental separation lead to an acute increase in the release of placental debris into the maternal circulation. To assess the effects of labour, samples were taken from 10 normal pregnant (NP) and 10 pre-eclamptic (PE) women at varied time points. Similarly to assess the effects of placental delivery, plasma samples were taken from 10 NP and 10 PE women undergoing elective caesarean section. There was a significant increase in the shedding of STBM in pre-eclampsia which was not seen in normal pregnancy and there was a small rise in STBM levels at placental separation in both normal pregnant and pre-eclamptic women undergoing caesarean section, but the differences were not significant. However, levels of placental cell-free corticotrophin releasing hormone mRNA were significantly increased in labour in both normal pregnancy and pre-eclampsia and were still high 24 h after delivery in the pre-eclamptic women. There was no significant increase in fetal or total DNA in labour, but the overall levels of total DNA (maternal and fetal) was increased in labour in pre-eclampsia compared to normal labour. The enhanced shedding of STBM and CRH mRNA in pre-eclampsia labour may have a role in cases of postpartum worsening of pre-eclampsia.     

Maternal plasma corticotrophin-releasing hormone—elevated in preterm labour but unaffected by indomethacin or nylidrin

Summary. The role of corticotrophin-releasing hormone (CRH) in preterm labour was studied in 23 women in preterm labour at between 26 and 33 weeks gestation who were randomly allocated to receive treatment with indomethacin (  n=11  ) or with nylidrin a beta-sympathomi-metic agent (  n=12  ). Maternal plasma CRH in the preterm group (median 70, range 9–597 pmol/1) before therapy was higher (   P < 0.05  ) than that in 23 control pregnancies, without uterine contractions, matched for gestational age (median 51, range 4–127 pmol/1). CHR levels determined after 3 and 24 h of treatment showed a 10% decrease in the indomethacin group and 10–20% decrease in the nylidrin group, but these changes were not statistically significant. After cessation of uterine contractions during tocolysis, 12 women proceeded to give birth preterm (<37 weeks) and their pretreatment CRH levels (median 195, range 9–597 pmol/1) were higher (   P < 0.05  ) than those in women whose pregnancy proceeded to term (median 52, range 16–207 pmol/1). In another group of women, full-term labour was not accompanied by any changes in maternal CRH levels. Umbilical plasma CRH levels were 1.1–9.8% of the paired maternal levels and did not rise with advancing gestational age. Nor had the type of delivery (elective caesarean section before labour, or preterm or term vaginal delivery) any effect on fetal CRH levels. Neither maternal nor fetal CRH was related to maternal or fetal cortisol levels. We conclude that: (i) maternal CRH is elevated in preterm labour, (ii) maternal CRH is not affected by treatment with indomethacin or nylidrin and (iii) fetal CRH is of no significance in the initiation of preterm or term labour.     

Modulation of hypothalamo-pituitary axis by stress during labor

OBJECTIVES: The present study is aimed to investigate the function of hypothalamo-pituitary-adrenal axis of women during late pregnancy and term labor. DESIGN: Levels of hormones were measured in blood of 34 women undergoing spontaneous labor and elective cesarean section, 2 days before and after delivery, and during labour. Additionally, blood from the umbilical vein and artery was also collected. MATERIALS AND METHODS: We have evaluated changes in corticotropin releasing hormone (CRH), adrenocorticotropin (ACTH) and dehydroepiandrosterone (DHEA) in vein blood of 34 subjects. The concentrations of hormones were measured by dint of RIA method. RESULTS: No significant correlation was found between hormone measurements and fetal outcome. CRH level in the umbilical vein was higher than in the umbilical artery, suggesting the placental origin of hormone. Prepartum CRH concentration was significantly higher in the group of spontaneously delivered patients. There were no correlations between CRH levels and ACTH and DHEA concentration in mother's blood plasma. In fetuses, higher prepartum CRH concentrations resulted in elevated levels of ACTH. No changes were found in DHEA concentration, in both mother and fetus. CONCLUSIONS: These results suggest that placental CRH may modulate a fetus's pituitary but not mother's. The observed high levels of this hormone play an important role mainly in preparation of mother and fetus for delivery.     

Maternal plasma corticotrophin-releasing hormone--elevated in preterm labour but unaffected by indomethacin or nylidrin

The role of corticotrophin-releasing hormone (CRH) in preterm labour was studied in 23 women in preterm labour at between 26 and 33 weeks gestation who were randomly allocated to receive treatment with indomethacin (n = 11) or with nylidrin a beta-sympathomimetic agent (n = 12). Maternal plasma CRH in the preterm group (median 70, range 9-597 pmol/l) before therapy was higher (P less than 0.05) than that in 23 control pregnancies, without uterine contractions, matched for gestational age (median 51, range 4-127 pmol/l). CHR levels determined after 3 and 24 h of treatment showed a 10% decrease in the indomethacin group and 10-20% decrease in the nylidrin group, but these changes were not statistically significant. After cessation of uterine contractions during tocolysis, 12 women proceeded to give birth preterm (less than 37 weeks) and their pretreatment CRH levels (median 195, range 9-597 pmol/l) were higher (P less than 0.05) than those in women whose pregnancy proceeded to term (median 52, range 16-207 pmol/l). In another group of women, full-term labour was not accompanied by any changes in maternal CRH levels. Umbilical plasma CRH levels were 1.1-9.8% of the paired maternal levels and did not rise with advancing gestational age. Nor had the type of delivery (elective caesarean section before labour, or preterm or term vaginal delivery) any effect on fetal CRH levels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Glucose production by the human placenta in vivo.

The human placenta transports glucose by facilitated diffusion down a concentration gradient from mother to fetus. It has previously been considered incapable of glucose synthesis. However, recent work has demonstrated the presence in placental tissue of glucose-6-phosphatase, which is required for the final step in the synthesis of glucose. Following continuous intravenous infusion into the maternal circulation of the stable isotope, 6,6-(2)H(2)glucose, during elective caesarean section, we have observed isotope dilution in the umbilical vein, without further dilution in the umbilical artery. Using a mathematical model containing maternal, placental and fetal compartments, the data were compatible with the release of glucose by the placenta. We conclude that the human placenta at term can produce glucose.     

Corticotrophin-releasing factor in human placenta: localization, concentration and release in vitro

Corticotrophin-releasing factor (CRF) immunoreactivity was demonstrated by immunohistochemical staining in the cytotrophoblast of the early pregnancy placenta, in the decidua and in the amnion. This localization is different from that of adrenocorticotrophic hormone (ACTH) and beta-endorphin, which are present in the syncytiotrophoblast. The release of immunoreactive CRF was demonstrated from both early and term placental tissues in vitro. The mean amounts of CRF in the early and term pregnancy placental/decidual extracts were 0.99 +/- 0.5 ng/g and 19.7 +/- 3.1 ng/g, respectively. A slightly greater amount of CRF was found in extracts from term placentae and in cord venous plasma collected after spontaneous vaginal delivery than in those collected at elective caesarean section performed before the beginning of labour.     

Differences in umbilical cord blood units collected during cesarean section,before or after the delivery of the placenta

Umbilical cord blood is largely employed as an alternative source of stem cells in the treatment of hemato-oncological diseases. Current results show that the success rate of purified umbilical cord blood engraftment is comparable to that obtained using bone marrow, and it is directly related to the number of pluripotent stem cells transplanted. The technique of fetal blood collection varies among different umbilical cord blood banks. Many authors collect umbilical cord blood during vaginal delivery, after placental detachment, while others collect it while the placenta is still within the uterus. In a previous randomized trial, we showed a greater collection of umbilical cord blood before placental detachment during vaginal delivery. The present study was performed to determine whether umbilical cord blood collection before placental detachment (group A) during cesarean section is superior to that after placental delivery (group B) puncturing the umbilical vein once and using a closed bag system. To accomplish this, 47 pregnant women subjected to cesarean section were enrolled in the study. Twenty-one of them were allocated to group A, while the remaining 26 formed group B. The volume of umbilical cord blood collected from the patients of group A was greater than that collected from patients of group B. The cord blood volume collected was 90.7 +/- 6.0 versus 60.9 +/- 13.7 ml; the cord blood nucleated cell number was 10.1 +/- 1.2 x 10(8) vs. 7.1 +/- 0.8 x 10(8); and the mean cord blood CD34+ cell number was 20.0 +/- 6.0 x 10(5) vs. 16.4 +/- 2.4 x 10(5), respectively.     

Umbilical cord serum activin A levels are increased in pre-eclampsia with impaired blood flow in the uteroplacental and fetal circulation

The aims of the present study were to evaluate the umbilical cord serum activin A concentrations in complicated pregnancies and also to explore the relationship between activin A levels and blood flow velocity in fetal arteries. Umbilical cord blood samples were obtained postpartum after a full term uneventful gestation (control group, n=40), and from pregnancies complicated by gestational diabetes (n=13), preterm labour (n=18), or pre-eclampsia (n=19). Cord serum activin A levels were three-fold higher in pregnancies complicated by pre-eclampsia (1.17+/-0.14 ng/ml, p<0.01) than in the control group (0.43+/-0.03 ng/ml), but were unaltered in the diabetes and preterm labour groups. The pre-eclampsia group had a marked increase of umbilical artery pulsatility index (PI) and also a decrease of middle cerebral artery PI (p<0.01). Furthermore, activin A concentration correlated directly with the umbilical artery PI (r=0.540, p=0.021), with the length of stay in the Neonatal Intensive Care Unit (r=0.857, p<0.001) and also with cord blood pH (r=-0.886, p<0.001). In conclusion, umbilical cord serum activin A levels are increased in the presence of pre-eclampsia and provide an indirect marker of impaired blood flow in the uteroplacental and fetal circulation.     

Altered gene expression in human placenta after suspected preterm labour

IntroductionSuspected preterm labour occurs in around 9% of pregnancies. However, almost two-thirds of women admitted for threatened preterm labour ultimately deliver at term and are considered risk-free for fetal development.MethodsWe examined placental and umbilical cord blood samples from preterm or term deliveries after threatened preterm labour as well as term deliveries without threatened preterm labour. We quantitatively analysed the mRNA expression of inflammatory markers (IL6, IFNγ, and TNFα) and modulators of angiogenesis (FGF2, PGF, VEGFA, VEGFB, and VEGFR1).ResultsA total of 132 deliveries were analysed. Preterm delivery and term delivery after suspected preterm labour groups showed similar increases in TNFα expression compared with the term delivery control group in umbilical cord blood samples. Placental samples from preterm and term deliveries after suspected preterm labour exhibited significantly increased expression of TNFα and IL6 and decreased expression of IFNγ. Suspected preterm labour was also associated with altered expression of angiogenic factors, although not all differences reached statistical significance.DiscussionWe found gene expression patterns indicative of inflammation in human placentas after suspected preterm labour regardless of whether the deliveries occurred preterm or at term. Similarly, a trend towards altered expression of angiogeneic factors was not limited to preterm birth. These findings suggest that the biological mechanisms underlying threatened preterm labour affect pregnancies independently of gestational age at birth.     

Prostaglandin E production by the fetal membranes in unexplained preterm labour and preterm labour associated with chorioamnionitis

The production of prostaglandin E (PGE) by amnion, choriodecidua and placenta was measured in 45 women delivered after spontaneous preterm labour, in 10 women delivered electively preterm, in 30 women at elective caesarean section at term, and in 28 women after spontaneous labour at term. In the preterm labour group 24 women had normal placental histology, and gestational age was 34 (31-36) weeks (median and range); 18 women had evidence of chorioamnionitis and gestational age was significantly shorter, 30 (24-36) weeks; three other patients had placental abruption. In the absence of inflammatory infiltration of these tissues the highest PGE output (fmol/mg dry weight/2 h) was found after labour at term and the lowest after uncomplicated preterm labour: 2640 (360-15,580) (median and range) compared with 1414 (164-11,045) in amnion, 677 (100-3245) compared with 308 (39-1086) in choriodecidua, and 1200 (520-3022) compared with 578 (150-1859) in placenta, respectively. Tissues showing chorioamnionitis produced much higher outputs of PGE from amnion (12,278, 1799-82,617) and from choriodecidua (1018, 216-11,768), but not from placenta (616, 89-4131). Chorioamnionitis seems to cause very early preterm labour by increasing PG production in the amnion and choriodecidua.     

Galanin concentrations in maternal circulation, amniotic fluid and umbilical cord blood during term labor: relationship with maternal body mass and neonatal birth weight.

BACKGROUND: Galanin is a hypothalamic regulatory peptide involved in the regulation of appetite. It is synthesized by the nervous system, anterior pituitary gland, adrenal medulla, pancreas, intestine and placenta. Placental secretion of galanin has until now only been investigated in animals. Additionally, galanin concentration has not been assessed in umbilical cord blood and amniotic fluid. PATIENTS AND METHODS: Galanin concentrations were measured in maternal circulation before term delivery, in cord blood and in amniotic fluid of 45 healthy pregnant women (gestational age 38 - 40 gestational weeks). The control group consisted of 26 normally menstruating healthy women. RESULTS: Plasma galanin concentrations were found to be similar in pregnant healthy women before term delivery (20.8 +/- 1.9 pg/ml) and non-pregnant women (19.0 +/- 1.7 pg/ml). Galanin concentration in umbilical cord blood (26.5 +/- 2.2 pg/ml) was significantly higher (p < 0.05) than in maternal circulation. Galanin concentration in amniotic fluid (20.4 +/- 1.0 pg/ml) was similar to that observed in maternal plasma, but significantly (p < 0.01) lower than in umbilical cord blood. A significant correlation was found between maternal body mass index and plasma galanin concentration (tau = 0.246; p < 0.05) and between birth weight and cord blood galanin concentration (tau = 0.345; p = 0.01). There was no significant correlation between placental mass and cord blood galanin concentration (tau = 0.124; p = 0.26). CONCLUSIONS: Plasma galanin concentration in pregnant women before term delivery is similar to that in non-pregnant women. The fetus rather than the placenta is the source of the high galanin concentration in umbilical cord blood. The role of galanin in the regulation of newborn weight is uncertain.     

Mode of collection does not influence haematopoietic content of umbilical cord blood units from caesarean deliveries

BACKGROUND: Collection strategy is the first step for collecting good quality cord blood units. There are two main different techniques for collecting cord blood from the umbilical vein: in the delivery room while the placenta is still in the utero by midwifes and obstetricians, or in an adjacent room after placental delivery by cord blood bank trained personal. Our aim was to evaluate the benefits and disadvantages between the two different cord blood collection strategies in caesarean deliveries. METHODS: We retrospectively analysed data of cord blood units collected from caesarean deliveries for a 3-year period. Caesarean section was performed with a low uterine transversal incision in all patients according to common obstetrical practice. Cord blood collection was performed before or after placental delivery. RESULTS: Obstetrical and umbilical cord blood data was obtained from 253 caesarean deliveries. No statistically significant difference was observed for obstetrical variables or cord blood variables except for Hct and platelets. CONCLUSIONS: We conclude both methods produce comparable TNC, CD34 and CFU counts of cord blood units collected from caesarean sections. Before placental delivery collection avoids the financial investment that generates the presence of cord blood banking personal in the maternity ward.     

Biologically active corticotropin-releasing hormone in maternal and fetal plasma during pregnancy

Corticotropin-releasing hormone was measured in the plasma of 110 pregnant women and in the umbilical cord plasma of 25 premature infants and 43 infants born at term. Mean maternal plasma corticotropin-releasing hormone was undetectable (less than 41 pg/ml) until mid-second trimester, rose to a mean of 204 +/- 24 pg/ml by 30 weeks' gestation, to 326 +/- 41 by 35 weeks, and then rose sharply near term, with a mean of 2930 pg/ml at 38 to 40 weeks' gestation. Sequential measurements in seven pregnant women confirmed that plasma corticotropin-releasing hormone rose in a predictable pattern, with a dramatic increase in the final weeks of pregnancy. There was little hour-to-hour variability in maternal plasma concentrations. Corticotropin-releasing hormone was also detectable in umbilical cord plasma; mean corticotropin-releasing hormone was 194 +/- 44 in the preterm infants and 150 +/- 19 in the term infants. The corticotropin-releasing hormone extracted from both the maternal and fetal circulation was biologically active in vitro and caused the dose-dependent release of adrenocorticotropic hormone and beta-endorphin from cultured rat anterior pituitary cells. A significant correlation was found between maternal plasma corticotropin-releasing hormone and cortisol levels the morning after betamethasone administration, a finding that supports a physiologic role for maternal plasma corticotropin-releasing hormone. We conclude that the placenta secretes large amounts of biologically active corticotropin-releasing hormone into both the maternal and fetal circulation during pregnancy. We demonstrate that this corticotropin-releasing hormone is secreted into the maternal plasma in a reproducible pattern during normal term pregnancy and suggest that sequential corticotropin-releasing hormone measurements may prove to be of clinical utility. In addition, placental corticotropin-releasing hormone may be an important modulator of the hypothalamic-pituitary-adrenal axis during pregnancy.     

Transplacental arteriovenous gradients for glucose, insulin, glucagon and placental lactogen during normoglycaemia in human pregnancy at term

The potential contributions of placental extraction and degradation to glucoregulatory hormone turnover in late pregnancy were assessed by measuring arteriovenous differences for glucose, insulin, glucagon and human placental lactogen (hPL) across the uterine and fetal circulation in ten pregnant women at the time of elective caesarean section. The observations were made during stable conditions of euglycaemia; values for maternal arterial glucose, insulin, glucagon and hPL were 78.8 +/- 5.0 mg/dl, 10.1 +/- 2.1 microU/ml, 72.0 +/- 8.5 pg/ml and 5.18 +/- 0.59 micrograms/ml, respectively. The glucose decrements observed consistently across the uterus and fetus indicated uptake by the placenta and fetus, and in the maternal circulation the arterial-uterine vein increment for hPL was 2.10 +/- 0.44 micrograms/ml. However, within the limits of analytical accuracy, no significant gradient could be demonstrated for insulin across the uterine (maternal) or umbilical (fetal) circulations. A small (8.5 per cent) but significant arteriovenous difference for glucagon was observed across the uterus but none was found on the fetal side of the placenta. The findings indicate that detectable gradients for insulin cannot be demonstrated under basal conditions of metabolism and at normal rates of placental blood flow. The results do not exclude the possibility of more significant extraction ratios under other physiological conditions or at higher concentrations of glucoregulatory hormones.     

Fetal placental vascular responses to corticotropin-releasing hormone in vitro. Effects of variation in oxygen tension

In this study, using the human placenta perfused in vitro with Krebs' bicarbonate solution, we have examined the effects of changes in oxygen tension on the vasoreactivity of fetal placental blood vessels to corticotropin releasing hormone (CRH). Vasodilatory responses to human synthetic CRH were measured during sub-maximal vasoconstriction of the fetal placental circulation with prostaglandin F(2alpha)(PGF(2alpha)) (1-100 micrometer). Decreases in fetal placental arterial perfusion pressure (FAP) were obtained with CRH under conditions of high oxygen or low oxygen tension, >/=450 mmHg and 相似文献   

The effect of labour and maternal oxytocin infusion on fetal plasma oxytocin concentration

It is not known whether human labour is associated with increased fetal oxytocin production or transfer of oxytocin across the placenta. Previous reports are contradictory, due in part, to the influence of maternal analgesia on fetal production. We determined plasma oxytocin concentration in the umbilical artery and vein of women after vaginal delivery and after caesarean section with general anaesthesia before or after the onset of labour. The results demonstrate that fetal production of oxytocin is not influenced by general anaesthesia, thus enabling comparison of labour and nonlabour samples at caesarean section. Labour was not associated with an increase in fetal oxytocin production. Oxytocin was also measured in the umbilical artery and vein during maternal oxytocin infusion to assess placental transfer. The results do not support transfer of oxytocin across the placenta in women.