Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Placentation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

Control of placental protein production by retinoic acid in cultured placental cells.

The synthesis of human chorionic gonadotropin (HCG), the subunit of HCG (HCG alpha), and pregnancy-specific beta 1-glycoprotein (PS beta G) was studied in temperature sensitive (ts), simian virus 40 (SV40) tsA mutant-transformed human first trimester placental (SPA255-26) cells. Retinoic acid increased the production of HCG and PS beta G but inhibited the production of HCG alpha in these cells. Passage of SPA255-26 placental cells in medium containing retinoic acid induced a stable altered phenotype characterized by elevated levels of HCG and PS beta G and a reduced level of HCG alpha. The retinoic acid induced phenotypic changes in these placental cells were reversible; removal of retinoic acid immediately decreased the production of HCG and PS beta G while increasing the production of HCG alpha. The ratio of HCG to HCG alpha in control SPA255-26 cells was approximately 0.1; this ratio increased to 4.8 in cells maintained in medium containing retinoic acid. Similarly, the HCG-to-HCG alpha ratio increased in choriocarcinoma cells maintained in retinoic acid containing medium. Our data suggest that retinoic acid may be needed to maintain a balanced production of HCG, HCG alpha, and PS beta G in placental cells in vitro. Retinoic acid may also play a role in modulating placental protein production during pregnancy.

Cell Differentiation↗

Alterations in fetal and placental deoxyribonucleic acid synthesis rates after chronic fetal placental embolization.

OBJECTIVE: Fetal growth and development are closely related to normal placental growth and function. We performed a study to determine the effect of a 10-day period of fetal hypoxemia induced by umbilical-placental hypoperfusion on tissue deoxyribonucleic acid synthesis rates in the 0.84 to 0.91 of gestation ovine fetus and placenta. STUDY DESIGN: Daily fetal placental embolization was performed in four chronically catheterized sheep fetuses until fetal arterial oxygen content decreased by approximately 30% compared with preembolization values. Five control fetuses received vehicle only. On experimental day 10, the deoxyribonucleic acid synthesis rate was determined by injecting tritiated thymidine (1 mCi/kg) intravenously approximately 8 hours before the end of the study. RESULTS: Fetal arterial oxygen decreased from 3.2 +/- 0.1 (SEM) mmol/L preembolization to 2.2 +/- 0.2 mmol/L on day 10 (p < 0.001) and remained unchanged in controls. On day 10 deoxyribonucleic acid synthesis rates were significantly reduced in embolized fetuses compared with controls, by 38% in cotyledons (83.0 +/- 15.1 vs 133.7 +/- 9.9 disintegrations/min/micrograms deoxyribonucleic acid, p < 0.05), 28% in the left ventricular wall (36.8 +/- 3.7 vs 51.0 +/- 4.7 disintegrations/min/micrograms deoxyribonucleic acid, p < 0.05), and 45% in the quadriceps muscle (15.4 +/- 4.0 vs 28.1 +/- 3.0 disintegrations/min/micrograms deoxyribonucleic acid, p < 0.05). Tritiated thymidine autoradiography demonstrated that cotyledonary deoxyribonucleic acid synthesis occurred exclusively in the fetal trophoblasts cells. CONCLUSION: We concluded that a reduction in cotyledonary, quadriceps muscle, and left ventricular myocardium deoxyribonucleic acid synthesis rates are the earliest adaptive mechanisms of fetal growth associated with development of umbilical-placental insufficiency. We speculate that alteration in the myocardial deoxyribonucleic acid synthesis rate could be a major contributing factor in the deterioration of fetal myocardial function associated with increased placental vascular resistance.

Analysis of Variance↗

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.

Animals↗

Expression of nitric oxide synthase in normal and preeclamptic placental tissue and effects of glyceryl trinitrate and shear stress on placental blood flow.

BACKGROUND: To study the expression of constitutively expressed nitric oxide synthase (cNOS) as well as the effects of glyceryl trinitrate (GTN) and shear stress on normal and preeclamptic placental tissue. METHODS: The expression of cNOS was studied using NADPH diaphorase activity reaction in seven normal and four preeclamptic placentas. The effect of GTN (n = 5) and shear stress induced by increasing the flow rate in the perfusion system (n = 5) was studied using an in vitro placental perfusion method. RESULTS: No difference in the distribution of cNOS in placental tissue was found between preeclamptic and normal pregnancies. Shear stress did not affect the production of nitric oxide metabolites. GTN was able to dilate placental vasculature. CONCLUSIONS: cNOS derived from syncytiotrophoblasts may not contribute to the development of preeclampsia. Placental vasculature responds to nitric oxide by vasodilation.

Blood Flow Velocity↗

Relationship between the changes in placental blood flow resistance assessed by Doppler technique and maternal serum placental aminopeptidases, which degrade vaso-active peptides, in pre-eclampsia.

Our study showed that there were statistically significant correlations between the systolic and diastolic ratio (S/D) of maternal uterine or umbilical artery and the levels of maternal serum aminopeptidase activities in pre-eclampsia. Kininase I was positively correlated with the S/D ratios, whereas placental leucine aminopeptidase (P-LAP) and aminopeptidase A were negatively correlated with the S/D ratios. It is known that the increased S/D ratios reflect the increased utero-placental blood flow resistance. Since our previous study showed that placental aminopeptidases degrade vasoactive peptides such as oxytocin, angiotensin and bradykinin, which the fetus actively produces, our present study suggests that the increased vascular resistance in feto-placental circulation in pre-eclampsia is partly controlled by changes in vaso-active peptides, via degradation by placental aminopeptidases.

Adult↗

15-Deoxy-Delta12,14-prostaglandin J2 and peroxisome proliferator-activated receptor gamma (PPARgamma) levels in term placental tissues from control and diabetic rats: modulatory effects of a PPARgamma agonist on nitridergic and lipid placental metabolism.

15-Deoxy-Delta(12,14)-prostaglandin J2 (15dPGJ2) is a peroxisome proliferator-activated receptor (3) (PPAR(3)) ligand that regulates lipid homeostasis and has anti-inflammatory properties in many cell types. We postulated that 15dPGJ2 may regulate lipid homeostasis and nitric oxide (NO) levels in term placental tissues and that alterations in these pathways may be involved in diabetes-induced placental derangements. In the present study, we observed that, in term placental tissues from streptozotocin-induced diabetic rats, 15dPGJ2 concentrations were decreased (83%) and immunostaining for nitrotyrosine, indicating peroxynitrite-induced damage, was increased. In the presence of 15dPGJ2, concentrations of nitrates/nitrites (an index of NO production) were diminished (40%) in both control and diabetic rats, an effect that seems to be both dependent on and independent of PPAR(3) activation. Exogenous 15dPGJ2 did not modify lipid mass, but decreased the incorporation of (14)C-acetate into triacylglycerol (35%), cholesteryl ester (55%) and phospholipid (32%) in placenta from control rats, an effect that appears to be dependent on PPAR(3) activation. In contrast, the addition of 15dPGJ2 did not alter de novo lipid synthesis in diabetic rat placenta, which showed decreased levels of PPAR(3). We conclude that 15dPGJ2 modulates placental lipid metabolism and NO production. The concentration and function of 15dPGJ2 and concentrations of PPAR(3) were altered in placentas from diabetic rats, anomalies probably involved in diabetes-induced placental dysfunction.

Acetates↗

Human placental gonadotrophin-releasing hormone-like factors: an artefact of human placental peptidases?

Non-denatured human placental cytosol fractions displaced tracer binding in parallel with gonadotrophin-releasing hormone (GnRH) isoform and agonist peptides in GnRH-specific radioimmunoassays and radioreceptor assays. However, placental immuno- and receptor binding-GnRH-like activity was highly correlated with inactivation of GnRH tracers, suggesting that placental GnRH-like factors may be an artefact of ligand degradation during assay. The properties and inhibitor sensitivities of the major (125)I-labelled GnRH-degrading enzymes of term placental cytosol were studied using a dextran-coated charcoal (DCC) adsorption assay as a rapid screen for GnRH tracer inactivation. Three different activities were demonstrable: (i) a cathepsin D-like enzyme (M(r) 55 kDa), active against all radiolabelled GnRH isoforms and agonists tested, optimal at acid pH, and inhibited specifically by pepstatin; (ii) a metallo-thiol endopeptidase activity (M(r) 70 kDa) optimal at alkaline pH (7-9) which degraded GnRH isoforms to a greater extent than GnRH analogues, inhibited dose-dependently by low concentrations of thiol reagents (N-ethylmaleimide, thimerosal), chelating agents (o-phenanthroline, EDTA), and by tosyl-phenylalanyl-chloromethyl ketone but not by other serine protease inhibitors; and (iii) a bacitracin-sensitive enzyme optimal at physiological pH. These observations permitted the development of a robust radioreceptor assay which minimized GnRH tracer degradation. Under these assay conditions, the GnRH-like radioreceptor assay activity of human placental cytosol fractions was markedly reduced.

Adsorption↗

Differential increase in the maternal serum concentrations of the placental proteins human chorionic gonadotrophin, pregnancy-specific beta 1-glycoprotein, human placental lactogen and pregnancy-associated plasma protein-A during the first half of normal pregnancy, elucidated by means of a mathematical model.

The present study was performed to compare the increase in maternal serum concentrations of four placental proteins during the first half of 240 normal pregnancies. The proteins were pregnancy-associated plasma protein-A (PAPP-A), human chorionic gonadotrophin (HCG), human placental lactogen (HPL) hormone, and pregnancy-specific beta 1-glycoprotein (PSG), all produced by trophoblast cells. The median increases were observed to be very close to exponential growth curves. Based on simple assumptions, these growth curves could be explained as being solely dependent on the growth of the placenta. The assumptions were that the proteins were produced in the placenta at a constant rate per gram of placental cell mass and secreted into the circulation shortly after synthesis. Our investigations showed that for two of the proteins, PSG and HPL, the rate constants were, in fact, close to the reported growth rate of the placenta, whereas the PAPP-A production rate constant was significantly higher than those of the others. The production curve for HCG was very different from that of the other proteins. PAPP-A and HCG must therefore have more complicated mechanisms for regulating the production. An equation was constructed that permitted estimation of the molar production of the placental proteins per gram of placental cell mass per day during the first half of normal pregnancy. The value was highest for HPL and lowest for PAPP-A.

Chorionic Gonadotropin↗

Diffusion characteristics of placental preparations affect the digoxin passage across the isolated placental lobule.

Our aim was to evaluate the isolated placental lobule to study maternofetal transplacental digoxin transfer and accumulation in placental tissue in vitro. Digoxin passage across the isolated lobule of 10 human placentas was calculated from repeated fetal and maternal perfusate samples, and placental tissue digoxin concentrations were measured at the end of the experiments. To determine the degree of overlap of the fetal and the maternal circulation, the antipyrine clearance was used. Digoxin disappearance from the maternal circuit was not significantly affected by the degree of overlap. In contrast, the increase of digoxin in the fetal compartment was significantly higher in "well-perfused" placentas (antipyrine clearance > 1.60 ml/min; n = 5) than in "malperfused" placentas (antipyrine clearance < 1.50 ml/min; n = 5) (end-feto to initial maternal digoxin ratio 0.44 +/- 0.08 vs. 0.30 +/- 0.08; p < 0.05), whilst the accumulation in placental tissue was higher in the latter group (0.45 +/- 0.07 vs. 0.62 +/- 0.10 ng/mg protein; p < 0.05). We conclude that the isolated placental lobule is suitable to quantify transplacental digoxin transfer in vitro, but the diffusion characteristics of each preparation have to be considered.

Anti-Arrhythmia Agents↗

Can placental surface area and neonatal weight be predicted from placental surface measurements? Preliminary observations on normal-term pregnancies.

OBJECTIVE: To evaluate the relations between chorionic plate measurements and neonatal weight as prerequisites for possible prediction of fetal weight using antenatal placental measurements. METHODS: We examined freshly delivered placentas. The surface area (chorionic plate) was measured using millimeter paper, and the two longest diameters (at right angles to each other) were determined (L1 and L2). The mean longest diameter [Lm = (L1 + L2)/2] was calculated. The relation of these diameters to neonatal and placental weight was studied. RESULTS: We examined 57 randomly selected placentas after normal pregnancy and delivery. The three chorionic plate diameters significantly correlated with the surface area and the placental and neonatal weights. The strongest correlation (r = 0.94; p < 10(-6) was found between Lm and placental surface area. CONCLUSIONS: Our preliminary results suggest that chorionic plate measurements may be suitable to predict placental surface area and neonatal birth weight in normal-term pregnancies. Further studies to verify prospectively these relations at various gestational ages and in cases of abnormal fetal growth are required.

Birth Weight↗

Influence of placental position on outcome in patients with placental abruption.

We retrospectively analyzed the clinical significance of placental position in patients with placental abruption by comparing cases in which the placenta was implanted on the anterior wall of the uterus (n=17) and those in which the placenta was on the posterior wall (n=12). There were no significant differences in clinical features of patients or pregnancy outcomes between the two groups. In this study, all patients with an anterior-wall placenta received a diagnosis of placental abruption prenatally, whereas only 8 patients (67%, p=0.01) with posterior-wall placenta received a diagnosis of placental abruption prenatally. Serious consideration should be given to the diagnosis of placental abruption in patients with a posterior-wall placenta.

Abruptio Placentae↗

Scintigraphic studies of uterine and placental growth and placental migration during pregnancy.

Placental scintigraphy with 113mIn (Indium) combined with cervical marking with a shielded 57Co (Cobalt) radioactive source was used to study uterine and placental growth in human pregnancy and placental location and migration in a total of 176 patients. Uterine length measurements can be used for selecting growth retarded fetuses. There was an approximately constant ratio between placenta diameter and uterine length (0.68 +/- 0.03). When the placenta was located on the ventral uterine wall, low implantation occurred in 61%. The corresponding figure for low implantation when the placenta was located on the dorsal uterine wall was 30%. The difference was highly significant. Placental migration was studied in 20 patients. Significant migration occurred in 11 cases. The placental margin closest to the internal cervical os migrated outwards about 3 cm on average.

Female↗

Prediction of low birth weight infants from ultrasound measurement of placental diameter and placental thickness.

BACKGROUND: The aim of the study was to help to predict low birth weight infants by measuring placental diameter and thickness. SUBJECTS AND METHODS: A prospective study was conducted of 70 consecutive singleton pregnancies to evaluate placental diameter and thickness by ultrasonographic measurement at 36 weeks gestation. The individual data were fitted to a logistic regression analysis. RESULTS: A "warning limit" of a placental diameter of 18 cm and placental thickness of 2 cm at 36 weeks gestation were calculated to predict low birth weight infants. CONCLUSION: Ultrasonographic placental diameter and thickness measurements appears to be of prognostic value in identifying the subsequent occurrence of fetal growth retardation.

Journal Article↗

Dual distant uterine placental insertion connected by a placental band. A case report.

BACKGROUND: There are several types of intrauterine membranes; most are not associated with any deleterious effect on fetal outcome. CASE: An unusual placental insertion was diagnosed sonographically at 23 weeks of gestation. It consisted of two distant placental insertions into the uterine wall, with a large placental mass between them floating freely in the uterine cavity. Normal fetal growth pattern and blood flow indices were found. A normal female neonate was delivered via low transverse cesarean section. There were no macroscopic or microscopic placental anomalies. CONCLUSION: This case raises several questions: the right mode of delivery, frequency of ultrasound follow-up and possibility of placental band rupture and hemorrhage during vaginal delivery.

Adult↗

Umbilical artery flow velocity waveforms and placental vascular resistance during maternal placental outflow obstruction in sheep.

This study was designed to test the hypothesis that the pulsatility index (PI) of the umbilical artery flow velocity waveform varies as a function of placental vascular resistance. Placental vascular resistance was raised by a one-minute occlusion of the maternal inferior vena cava. Occlusion of the maternal inferior vena cava resulted in a decrease in fetal heart rate from 183 +/- 7.8 beats/min to 142 +/- 8.6 beats/min at the end of occlusion (P less than 0.05). Placental vascular resistance increased from 0.113 +/- 0.021 mmHg.ml-1.min during control to 0.151 +/- 0.033 mmHg.ml-1.min (P less than 0.05) during occlusion. The pulsatility index increased from 1.05 +/- 0.05 to 1.85 +/- 0.4 (P less than 0.05) during occlusion. After parasympathetic blockade with atropine fetal heart rate did not change during occlusion. Placental vascular resistance increased from 0.091 +/- 0.014 before to 0.121 +/- 0.021 mmHg.ml-1.min during occlusion (P less than 0.05). The pulsatility index increased from 0.98 +/- 0.1 before to 1.12 +/- 0.12 during occlusion (P less than 0.05). These results support the hypothesis that, in the fetal sheep, placental vascular resistance is one of the determinants of the pulsatility index of the umbilical artery.

Animals↗

Placental mono-oxygenation: characteristics and partial purification of a hematin-activated human placental mono-oxygenase.

Human placental mono-oxygenase activities were markedly increased after additions of micromolar quantities of hematin to reaction vessels. The magnitude of the increases diminished with increasing (induced) levels of hematin-independent activity. The activating effect of hematin could be observed in unbroken cell preparations, in whole homogenates, and in various subcellular fractions. Highest hematin-dependent activity was measured in microsomal fractions of placental homogenates. With benzo(a)pyrene as substrate, response to the stimulatory effect of hematin in human placental preparations was not as profound as that observed in monkey or rabbit placentas but was more marked than the responses observed in placental preparations from rats or mice. Hematin-activated mono-oxygenase activity present in washed microsomal fractions of human placental homogenates could be solubilized with detergents, the most effective of which was Triton N-101. The solubilized activity also could be partially purified by polyethylene glycol fractionation. Attempts to further purify, however, resulted in loss of activity. All results were consistent with the hypothesis that the effect of hematin is mediated via reconstitution of hematin-free apocytochrome(s) P-450.

Animals↗

Patterns of placental injury. Correlations with gestational age, placental weight, and clinical diagnoses.

Given the dependence of the fetus on adequate placental function, one might predict that specific placental lesions would be associated with distinct pregnancy outcomes. To test this hypothesis, we examined 609 nontwin placentas and explored the relationship between histologic diagnosis and the following variables: gestational age at delivery, placental size, and selected categories of clinical disease. Five separate patterns of placental injury were examined. Two lesions were particularly frequent prior to 37 weeks' gestation: increased intervillous fibrin, which was most common in early preterm placentas (20 to 31 weeks), and membrane hemosiderin, which was increased in both early and late preterm placentas (32 to 36 weeks). Three lesions--maternal vasculopathy, villitis of unknown etiology, and increased intervillous fibrin--were associated with retarded fetal and placental growth. Only maternal vasculopathy was significantly increased in placentas from pregnancies with gestational hypertension, while two other lesions--villitis of unknown etiology and increased intervillous fibrin--were appreciably increased with nonhypertensive chronic antenatal abnormalities.

Female↗

Placental site trophoblastic tumor: human placental lactogen and pregnancy-associated major basic protein as immunohistologic markers.

Placental site trophoblastic tumor (PSTT) consists of a neoplastic proliferation of intermediate or extravillous trophoblast (also known as X cells). Pregnancy-associated major basic protein (pMBP) is a marker for placental intermediate trophoblast. We compared the distribution of pMBP and human placental lactogen (hPL) in 24 PSTT and 3 exaggerated placental site (EPS) specimens using two distinct immunohistologic methods. Statistical analyses were used to compare staining intensities in metastatic and nonmetastatic lesions. By immunofluorescence, 77% of the PSTT specimens and 100% of the EPS specimens stained with antibodies to pMBP, and the pMBP was localized in intermediate trophoblast and surrounding extracellular areas. By immunohistochemistry, 78% of the PSTT specimens and 100% of the EPS specimens stained for pMBP with a pattern comparable with that of immunofluorescence. Likewise, by immunohistochemistry, hPL stained 96% of the PSTT specimens and 100% of the EPS specimens. Immunohistochemical staining intensities for pMBP and hPL correlated (r2 = +.24; P = .013), but hPL staining was mainly confined to intermediate trophoblast and was more intense. Anti-pMBP tended to stain metastatic PSTT weakly. Thus, pMBP is a useful marker for intermediate trophoblast tumors and could help distinguish these from other forms of trophoblastic disease.

Adult↗