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PubMed1976

[The ratio birth-weight, placental weight and the term of delivery. A contribution to the problem of a relative placental insufficiency in late pregnancy (author's transl)].

It is suggested, that a relative placental insufficiency in late pregnancy is one of the releasing factors of childbirth. Under this assumption 1027 deliveries in term pregnancy (266th-294th day of pregnancy) were inquired on the interrelationship between the ratio brith-weight: placental-weight and the duration of pregnancy. The average birth-weight increases slighly but significantly with the duration of pregnancy just as the average placental-weight. The average ratio birth-weight: placental-weight decreases significantly: The more unfavorable the ratio birth-weight: placental-weight is, the shorter remains the fetus in utero. This underlines the assumption of a relative placental insufficiency as one of the releasing factors of childbirth.

Birth Weight↗
PubMedDate not supplied

Immunolocalization of basic fibroblast growth factor (bFGF) in growing and growth-inhibited placental cells: a possible role for bFGF in placental cell development.

The distribution of basic (b) fibroblast growth factor (FGF) in growing and growth-arrested human placental tumour cells, as well as normal placental villous trophoblasts, was studied by immunofluorescence microscopy with antibodies to the amino terminus of bFGF. Placenta (FAR, FEG-3), breast (MCF-7, T-47D), cervix (HeLa) and uterine (HEC-1-A) tumour cells showed the same two patterns after immunofluorescent staining with antibodies to bFGF: (i) a perinuclear pattern and (ii) an intense homogeneous staining of the nucleus and cytoplasm. The homogeneous bFGF staining pattern was associated predominantly with actively dividing cells, observed at different stages of mitosis and cytokinesis. Placental (FEG-3) cell division was inhibited with methotrexate (MTX), a chemotherapeutic agent used in the treatment of placental tumours. MTX-treated FEG-3 cells as well as 'normal' non-proliferative placental (syncytiotrophoblast) cells from term placentae, showed perinuclear staining with antibodies to bFGF and immunofluorescence microscopy. The nuclear localization of bFGF in dividing but not non-dividing placental cells, suggests a role for bFGF in cytotrophoblast proliferation in vivo.

Cell Nucleus↗
PubMed2006

Altered placental syncytin and its receptor ASCT2 expression in placental development and pre-eclampsia.

OBJECTIVE: To investigate the alterations of syncytin, a fusogenic membrane protein involved in syncytiotrophoblastic layer formation, and its receptor ASCT2 expression in placental development and pre-eclampsia. DESIGN: Analyses of syncytin and ASCT2 expression in placentas from different stages of pregnancy and women with pre-eclampsia and in cytotrophoblasts cultured in normoxic and hypoxic conditions. SETTING: Placental samples were collected from a tertiary medical centre. POPULATION: Sixteen women with pre-eclampsia and 58 pregnant women presented as pregnancy (5-19 weeks of gestation) for elective termination, preterm birth, or normal term delivery. METHODS: The quantitative real-time polymerase chain reaction was used to study the syncytin and ASCT2 expression during placental development in 35 placentas from women without pre-eclampsia (ranged from 5 to 40 weeks of gestation) and the alterations of pre-eclamptic placentas (n=16) compared with gestational-age-matched controls (n=16). Western blot analysis was performed to study the protein level of syncytin in pre-eclamptic placentas and gestational-age-matched controls. The hypoxic effect on trophoblastic syncytin and ASCT2 expression was further studied in cytotrophoblasts cultured in 2% oxygen (n= 7). MAIN OUTCOME MEASURES: Syncytin and ASCT2 messenger RNA (mRNA) in placental tissue and cytotrophoblasts. RESULTS: The level of syncytin mRNA expression increased significantly since the first trimester of pregnancy until 37 weeks of gestation, when the level of syncytin expression was reduced. The ASCT2 mRNA expression was decreased significantly since the second trimester and was relatively stable since then to 40 weeks of gestation. Furthermore, a significant reduction in syncytin mRNA expression was observed in pre-eclamptic placentas and cytotrophoblasts cultured in hypoxia, but not a reduction in ASCT2 mRNA expression. Correlatively, the protein level of syncytin was decreased in pre-eclamptic placentas. CONCLUSIONS: A reduced placental expression of syncytin but not ASCT2 may contribute to altered cytotrophoblastic cell fusion processes and disturbed placental function in pre-eclampsia. Correspondingly, hypoxia decreases syncytin but not ASCT2 gene expression in cultured cytotrophoblasts.

Amino Acid Transport System ASC↗
PubMed1991

Placental lactogen secretion during prolonged-pregnancy in the rat: the ovary plays a pivotal role in the control of placental function.

The serum of rats at mid-pregnancy contains at least 2 distinct placental lactogen (PL)-like substances tentatively termed placental lactogen-alpha (PL-alpha) and placental lactogen-beta (PL-beta) (Endocrinol Japon 38: 533-540, 1991). We have investigated the secretory patterns of three placental lactogens (PL-alpha, PL-beta and placental lactogen-II) during normal pregnancy and in two prolonged-pregnancy models. Pregnancy was prolonged by the introduction of new corpora lutea by inducing ovulation on day 15 of pregnancy by successive treatments with PMSG (30 IU/rat, sc on day 12) and hCG (10 IU/rat, iv on day 14), and in the second model by progesterone implants on day 15 of pregnancy. During normal pregnancy, each of the 3 PLs exhibited only one secretory peak in the serum; PL-alpha and PL-beta on day 12 and placental lactogen II (PL-II) on day 20. Interestingly, in the rats with new sets of corpora lutea, serum PL-alpha and PL-beta levels began to increase again on day 18 and showed peaks on day 20 for PL-alpha and on day 22 for PL-beta. In this model, the initiation of PL-II secretion was not affected, but high levels were maintained until day 26, when parturition occurred. In rats receiving either PMSG or hCG, the secretory patterns of the PLs were similar to as those during normal pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1985

Effect of restriction of placental growth on the concentrations of insulin, glucose and placental lactogen in the plasma of sheep.

The effect of restricting placental growth on maternal glucose, insulin and placental lactogen was investigated in 16 ewes carrying singleton lambs. Uterine caruncles were removed from seven ewes (caruncle ewes) before pregnancy, resulting in reduced placental size and retarded intra-uterine fetal growth. The concentration of insulin in maternal plasma was similar in both control and caruncle ewes. The concentration of glucose was significantly higher in the caruncle than in the control ewes (3.26 +/- 0.15 (S.E.M.) mmol/l, number of observations (n) = 9, vs 2.75 +/- 0.1, n = 9, P less than 0.02, and 3.27 +/- 0.16, n = 7, vs 2.46 +/- 0.11, n = 12, P less than 0.001, for the carotid artery and utero-ovarian vein respectively). The concentration of ovine placental lactogen (oPL) in the utero-ovarian vein was reduced in the caruncle compared with the control ewes (283 +/- 65 micrograms/l, n = 8, and 705 +/- 106 micrograms/l, n = 18, P less than 0.02, respectively). Restriction of placental growth by removal of endometrial caruncles similarly reduced the concentrations of oPL in maternal arterial plasma (231 +/- 54 micrograms/l, n = 9, and 621 +/- 96 micrograms/l, n = 18, P less than 0.002). Production of oPL by the placenta was also reduced by limiting placental growth to 30 +/- 11 micrograms/min, n = 8, compared with 133 +/- 43 micrograms/min, n = 15, P less than 0.05, for the controls. Production of oPL per gram of placenta in the caruncle group, although only 34% of the control value, was not reduced significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Relations between maternal and fetal plasma concentrations of placental lactogen and placental and fetal weights in well-fed ewes.

The concentration of ovine placental lactogen (oPL) in maternal plasma varies with litter size and nutritional status, making it difficult to compare these concentrations across studies. In this study, 27 Dorset and Finn-Dorset crossbred ewes with litters of known size and gestational age were used to relate concentrations of oPL in maternal plasma to placental and fetal weights. Fetal oPL concentrations also were correlated to these variables in 12 chronically catheterized singleton fetuses. The concentration of oPL in maternal plasma increased with increasing placental weight across litter sizes ranging from 1 to 3 (r = .716). When expressed per gram of placenta, oPL was greater (P less than .05) in those ewes carrying multiple fetuses. There was no correlation between maternal and fetal oPL in time-matched samples or in average values between individuals for ewes carrying singleton pregnancies. Within the singleton group, placental weight and fetal weight were well correlated (r = .761), as were the concentration of fetal plasma oPL and fetal weight (r = .699). Placental weight plus fetal oPL could explain 81% of the variation seen in fetal weight. These results imply that maternal and fetal oPL release are controlled independently and that fetal oPL affects fetal growth by a mechanism not directly related to placental size.

Animals↗
PubMed2000

Effect of a high maternal dietary intake during mid-gestation on components of the utero-placental insulin-like growth factor (IGF) system in adolescent sheep with retarded placental development.

The aim of the present study was to investigate the effects of administering a high plane diet during early to mid-gestation on the uterine and placental insulin-like growth factor (IGF) system and on systemic IGF-I concentrations in pregnant adolescent ewes with restricted placental growth. Embryos recovered from superovulated ewes inseminated by a single sire were transferred in singleton to the uterus of adolescent recipients. After transfer ewes were offered a high (H) or moderate (M) amount of a complete diet calculated to promote rapid or normal maternal growth rates, respectively. Five ewes from each group were switched from either M to H or H to M diets at day 52 of gestation. Maternal and fetal blood samples and placental tissues were collected from all animals at day 104. Ewes on the high plane diet from mid-gestation (HH, MH groups) had restricted placental mass (P < 0.01) and tended to have smaller fetuses. This was associated with increased maternal plasma IGF-I concentrations (P < 0.001). The pattern of expression of components of the IGF system in the uterus and placenta was studied by in situ hybridization. IGF-I mRNA concentrations were below the limit of detection. IGF-II mRNA expression was high in the fetal mesoderm and present in maternal stroma, but was not influenced by nutritional treatment. In contrast, IGF binding protein 1 (IGFBP-1) mRNA expression was higher (P < 0.05) and IGFBP-3 mRNA expression was lower (P < 0.05) in the endometrial glands of ewes in HH and MH groups. In the fetal trophoblast, IGFBP-3 mRNA expression was higher in the MH group. Type 1 IGF receptor expression was increased (P < 0. 01) in the luminal epithelium of the HM group and IGFBP-2 mRNA expression was highest in the placentome capsule of ewes in the HH group. Together, these results indicate that reprogramming of the uterine and placental IGF axis by maternal nutrition could contribute to placental growth retardation in growing adolescent sheep.

Animal Nutritional Physiological Phenomena↗
PubMed2003

Myometrial and placental artery reactivity alone cannot explain reduced placental perfusion in pre-eclampsia and intrauterine growth restriction.

OBJECTIVES: (1) To investigate a possible association between myometrial and placental artery vasoreactivity and perfusion at the basal and chorionic plates, respectively. (2) To confirm that myometrial arteries from women with pre-eclampsia and intrauterine growth restriction exhibit an attenuated endothelium-dependent vasodilatory response. METHODS: Women with normal pregnancy, pre-eclampsia and intrauterine growth restriction had a magnetic resonance scan to assess placental perfusion using a technique called intravoxel incoherent motion. At delivery, myometrial and chorionic plate placental arteries were assessed on a wire myograph. Vessels were pre-constricted with the thromboxane mimetic U46619 and dilated with incremental doses of bradykinin. RESULTS: Pre-constricted myometrial arteries from women with pre-eclampsia or intrauterine growth restriction exhibited an attenuated vasodilatory response to bradykinin, compared with normal pregnancy (P < 0.0001). Pre-constricted placental arteries exhibited a minimal vasodilatory response in all three groups of women (P = 0.10). Maximal constrictor and vasodilatory responses of myometrial arteries were not associated with the perfusing fraction at the basal plate. Maximal constrictor and vasodilatory responses of chorionic plate placental arteries were not associated with the perfusing fraction at the chorionic plate. CONCLUSION: We confirm that myometrial arteries from women with pre-eclampsia or intrauterine growth restriction exhibit an attenuated endothelium-dependent vasodilatory response. Apart from vasoreactivity of small arteries, other factors may be involved in the control of placental perfusion.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1990

Response of placental vasculature to high glucose levels in the isolated human placental cotyledon.

We report the effect of high glucose infusion on vascular resistance in isolated human placental cotyledons perfused with Krebs-Ringer-bicarbonate solution containing 80 mg/dl (4.4 mmol/L), 160 mg/dl (8.8 mmol/L), or 320 mg/dl (17.6 mmol/L) D-glucose (n = 6). Placental vascular resistance remained constant during 25-minute perfusion periods with 80 mg/dl followed by 160 mg/dl glucose solution. Subsequent perfusion with 320 mg/dl glucose produced a significant increase in placental vascular resistance. Placentas were also studied in which the placental cotyledon was sequentially perfused for 25-minute periods with solutions containing glucose at 80 mg/dl followed immediately by 320 mg/dl (n = 5). Placental vascular resistance remained constant throughout perfusion with 80 mg/dl glucose solution but increased significantly after beginning perfusion with 320 mg/dl glucose. We conclude that the increase in placental vascular resistance appears to be a function of the high glucose level rather than the duration of glucose perfusion.

Arteries↗
PubMed1992

Placental aryl hydrocarbon hydroxylase activity and placental calcifications.

Induction of aryl hydrocarbon hydroxylase (AHH) activity in the placenta as a result of maternal exposure to polycyclic aromatic hydrocarbons contained in cigarette smoke has been well documented. Furthermore, calcifications are more prevalent in the placentas of pregnant smokers than in those of non-smokers. The present study examines whether this latter relationship could be explained by the induction of AHH activity in the placenta. AHH levels were determined at birth in 141 unselected pregnant women admitted for delivery. Macroscopic placental examination was performed for vascular lesions, abnormalities of placental shape, of the cord and parameters of placental maturity such as basal and parenchymatous calcifications. Significant increases in the prevalence of calcifications of the placental basal plates and parenchyma with the induction of placental AHH were found. A similar significant association between smoking and AHH activation was also observed. These findings remained unchanged when controlling for smoking status assessed both by questionnaire and presence of cotinine in mother's urine. Moreover, the apparent association between smoking 'factor' and calcifications disappeared when controlling for AHH induction. Therefore, the association between smoking and placental calcifications previously related could be mediated by the AHH induction.

Aryl Hydrocarbon Hydroxylases↗
PubMed1995

Human placental endothelin: expression of endothelin-1 mRNA by human placental fibroblasts in culture.

Endothelin-1 (ET-1) mRNA is expressed by the human placenta in a developmentally regulated manner and has been shown to stimulate the growth of placental mesenchymal cells. The ability of placental fibroblasts to express preproET-1 mRNA was studied to determine if ET-1 could potentially participate via autocrine mechanisms in the proliferation of placental fibroblasts. Fibroblasts were isolated from normal placentae at various gestational ages (7-19 weeks and term) and their abilities to express preproET-1 mRNA in culture evaluated by Northern analysis. Sparse, rapidly growing cultures of placental fibroblasts expressed preproET-1 mRNA at each gestational age in the presence of 10% FBS. The regulation of preproET-1 expression in placental fibroblasts was studied by exposing cells to known mitogenic stimuli. Quiescent, confluent monolayers of placental fibroblasts expressed no detectable levels of preproET-1 mRNA under basal conditions. Epidermal growth factor (EGF, 10 mg/ml), transforming growth factor-beta 1 (TGF-beta 1, 5 ng/ml), or interleukin 1 beta (IL-1 beta) alone, had no significant effect on steady state preproET-1 mRNA levels. Cycloheximide, an inhibitor of protein synthesis, increased the steady state levels of preproET-1 mRNA at a concentration of 10 micrograms/ml. In the presence cycloheximide, IL-1 beta markedly stimulated preproET-1 mRNA expression, whereas EGF was less effective. TGF-beta 1 had no effect in the presence or absence of cycloheximide. In contrast, 12-O-tetradecanoylphorbol 13-acetate (TPA, 20 nM) exerted a small stimulatory effect on preproET-1 mRNA expression which was not influenced by cycloheximide.(ABSTRACT TRUNCATED AT 250 WORDS)

Blotting, Northern↗
PubMedDate not supplied

An examination of whether human placental perfusion allows accurate prediction of placental drug transport: studies with diazepam.

INTRODUCTION: Presently, no well-validated predictive tools are available for human placental transfer. We studied the transplacental passage of diazepam (DZP) in a recirculating dual human placental perfusion and compared the data with in vivo clinical data from the literature. METHODS: Term placentas from healthy mothers without medication were used. The dual, recirculating perfusion technique was used. DZP (2 microg/ml, n = 4; 200 ng/ml, n = 3) and the reference compound antipyrine (100 microg/ml) were added into the maternal circulation simultaneously. The disappearance of drugs from the maternal circulation and appearance into the fetal circulation were followed every 15 min for 2 h. RESULTS: DZP was detectable in the fetal circulation within 15 min in all of the perfusions indicating rapid transfer. DZP concentrations in the maternal circulation were higher than in the fetal circulation throughout the perfusion with both initial concentrations. At the end of the perfusion, the feto-maternal ratio was 0.48 +/- 0.11 (mean +/- S.D.) and the transfer from the maternal to the fetal compartment 18.4 +/- 3.6% with 2 microg/ml of DZP and 0.55 +/- 0.10 and 20.5 +/- 3.1% with 200 ng/ml of DZP, respectively. DZP concentrations in the perfused area of the placenta were in average 2 times higher than in the maternal perfusate and 3.6 times higher than in the fetal perfusate. Total recovery of DZP from samples, perfusion fluid, and perfused tissue was 37.6 +/- 21%. DISCUSSION: Since animal studies in vivo do not accurately predict human placental transfer and it is problematic to study placental transfer of drugs in humans in vivo, the present human placental perfusion system could serve as one part of a test battery for fetotoxicity. However, although our earlier studies and those from the literature indicate a good correlation between in vivo and placental perfusion data, the present study shows this is not the case for all drugs.

Anticonvulsants↗
PubMed2001

Quantitative digital analysis of regional placental perfusion using power Doppler in placental abruption.

PURPOSE: To apply digital imaging techniques to the quantification of placental vascularity using power Doppler. MATERIALS AND METHODS: Regional placental blood flow was measured in a case of large placental abruption, shortly after presentation and 1 week later. Images were stored digitally and analysed using purpose-designed software (CQ Analysis) to extract and measure vascular energy information. The integrated color energy (ICE) was determined in the main body of placental tissue and in a cotyledon isolated by the retroplacental clot. RESULTS: Initial assessment at 25 weeks showed only a small difference in integrated energy between normal placenta and the isolated cotyledon (ICE ratio 1.44, P < 0.04). One week later, perfusion in the isolated cotyledon had fallen both on qualitative and quantitative assessment (ICE ratio 3.98, P < 0.0001). This area subsequently became devascularized. CONCLUSION: Placental perfusion may be quantified using digital power Doppler analysis. Further studies are indicated to evaluate its role in assessing regional and/or global placental perfusion as well as fetal organ perfusion.

Abruptio Placentae↗
PubMed2003

Longitudinal serum concentrations of placental growth factor: evidence for abnormal placental angiogenesis in pathologic pregnancies.

OBJECTIVE: Complicated pregnancies demonstrate abnormal decidual and placental villous vasculature. We examined maternal concentrations of vascular endothelial growth factor and placental growth factor in normal pregnancies and in pregnancies that were complicated by isolated idiopathic small-for-gestational-age (SGA) newborn infants, preeclampsia alone, or preeclampsia with SGA newborn infants at the time of clinical disease and before the onset of clinical signs. STUDY DESIGN: Serum vascular endothelial growth factor and placental growth factor were measured by enzyme-linked immunosorbent assay in cross-sectional and longitudinal cohorts of pregnant nulliparous women. The results were compared by Wilcoxon tests or a mixed-models method, respectively. RESULTS: In the cross-sectional study, serum placental growth factor was reduced in abnormal pregnancy relative to control subjects (SGA newborn infants, 18 [P =.04]; preeclampsia, 20; or preeclampsia with small- for-gestational-age newborn infants, 11 [P =.0001]) as early as 15 to 19 weeks of gestation in preeclampsia with SGA newborn infants. Vascular endothelial growth factor was <30 pg/mL in all serum specimens from pregnant women. CONCLUSION: We postulate that decreased placental growth factor production results in abnormalities of placental angiogenesis through direct and indirect effects on other vasculotropic growth factors.

Adult↗
PubMed1978

The effect of litter size on placental blood flow and placental calcium transfer in the multifoetate guinea-pig.

1. Placental blood flow rate and calcium transfer rate were measured at 61 d of pregnancy in guinea-pigs carrying between one and eight foetuses. 2. Placental blood flow rate was significantly correlated with foetal weight. Ca transfer rate was related to placental size. Irrespective of litter size the mean amount of Ca transferred across a placenta was between 0.22 and 0.34 mg/h per g placental tissue. 3. It was concluded that there was a limit to the rate of transfer which was produced by a combination of limitations in placental blood flow rate, maternal plasma Ca concentration and placental tissue transfer capacity.

Animals↗
PubMed1992

Placental bed biopsies in placental abruption.

OBJECTIVE: To investigate structural changes in the uteroplacental blood vessels in association with placental abruption. DESIGN: Prospective descriptive study. SUBJECTS: 18 women with clinical evidence of severe placental abruption delivered by caesarean section. INTERVENTIONS: Placental bed biopsies were obtained at caesarean section and studied histologically. RESULTS: Six specimens did not include trophoblast in the myometrium and were therefore not representative of the placental bed. Of the 12 representative specimens, seven demonstrated absence of physiological transformation of the utero-placental arteries (four of these were from hypertensive patients). Four biopsies showed abnormal vascular structures deep in the myometrium. One of these abnormal vessels included a fresh plug and extensive surrounding intramyometrial haemorrhage. CONCLUSIONS: Vascular malformations in association with placental abruption may be the result of trophoblastic invasion and could be the site of vessel rupture. Further descriptive and comparative studies are needed.

Abruptio Placentae↗
PubMed1993

Glucocorticoid suppression of human placental fibronectin expression: implications in uterine-placental adherence.

Increased levels of glucocorticoids are associated with human parturition whether occurring before or at term. In the present study we examined the effects of glucocorticoids on placental fibronectin (FN) expression in cytotrophoblasts, isolated from human term placentas, to provide a potential mechanism through which glucocorticoids may influence uterine-placental adherence near parturition. Based on immunoassays, relative to controls, media levels of placental FNs bearing an oncofetal epitope (onfFN) were inhibited 65-80% by treatment with 10(-7) M dexamethasone (DEX) during experiments in which cumulative levels and daily release of onfFN were measured. DEX treatment increased human CG production by cytotrophoblasts approximately 3-fold without affecting the levels of total protein, suggesting that DEX treatment did not reduce placental function. DEX and cortisol inhibited onfFN expression with an EC50 of 2 and 16 nM, respectively. Other steroids were not effective in down-regulating onfFN expression, indicating that this was a glucocorticoid-specific response. In immunoprecipitation studies, treatment of cytotrophoblasts with 10(-7) M DEX for 3 days inhibited both release of labeled FN to the media and its incorporation into cell-associated material by approximately 80%. Results from Northern blotting indicated that DEX treatment suppressed levels of FN messenger RNA approximately 90% relative to controls. Levels of labeled laminin in media were inhibited approximately 80% by a 3-day treatment with 10(-7) M DEX, suggesting that glucocorticoids may coordinately suppress the synthesis of multiple extracellular matrix proteins in cytotrophoblasts. In our model, we propose that glucocorticoids may suppress placental extracellular matrix protein synthesis, which could lead to decreased uterine-placental adherence and be associated with parturition.

Blotting, Northern↗