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At least 865 records · Page 48Linked to original sources
PubMed1994

Reduced thromboxane receptor affinity and vasoconstrictor responses in placentae from diabetic pregnancies.

Thromboxane has been implicated in the pathogenesis of maternal hypertension in high-risk pregnancies, but potential abnormalities in thromboxane-mediated constriction of fetoplacental vessels has not been examined. Using the isolated perfused fetoplacental cotyledon, we compared the vasoconstrictor responses to a thromboxane mimetic, U46619, in placentae from normal women and women with diabetes mellitus (classes C, D and R). Increases in perfusion pressure in response to bolus injections of U46619 were used to construct dose-response curves. The threshold dose of U46619 to cause a pressor response was similar in placentae from normal and diabetic pregnancies, but the slope of the dose-response curve was decreased by 39 per cent in placentae from diabetic pregnancies compared with normal controls (P < 0.01). To examine the potential contribution of altered thromboxane receptors, equilibrium binding studies were performed using the thromboxane antagonist [3H]-SQ29548 to a 44,000 g fraction of placental homogenate. The affinity of thromboxane receptors was significantly decreased in placentae from diabetic pregnancies compared with normal controls [Kd = 41.9 +/- 7.9, (n = 6) versus control, 21.4 +/- 1.3 nM (n = 26), P < 0.001]. In contrast, the density of thromboxane receptor sites was not significantly changed (diabetes, 176.0 +/- 6.2 versus control, 150.3 +/- 6.5 fmol/mg, P = not significant). Placental production of thromboxane and prostacyclin were measured by the incorporation of [14C]-arachidonic acid into [14C]-thromboxane B2 and [14C]-6-keto-prostaglandin F1 alpha, respectively. Incorporation of [14C]-arachidonic acid into both thromboxane B2 and 6-keto-prostaglandin F1 alpha was similar in placentae from diabetic and normal pregnancies. We conclude that vascular responsiveness to thromboxane is reduced in placentae from mothers with diabetes by a receptor-mediated mechanism. These changes may contribute to abnormalities in the regulation of fetoplacental haemodynamics, growth and development in pregnancies complicated by diabetes mellitus.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1994

Release of lipid from the equine placenta during in vitro incubation.

An in vitro incubation technique was used to examine release of lipids from the equine placenta. Placental tissue was obtained at term (n = 5, term = 320-365 days) and earlier in gestation (n = 8, mean = 266 days). Term placentae were incubated at two temperatures, 4 degrees C (control) and 37 degrees C for 2 h. Pre-term placentae were incubated at 37 degrees C with two different concentrations of fatty acid in the medium. Tissues and media were analysed for their lipid concentrations. Term and pre-term placentae released free fatty acid (FFA) and phospholipid into the incubation medium during incubation at 37 degrees C. Long chain polyunsaturated fatty acids derived from the essential fatty acids were released into the media. The fatty acid profiles of the lipids released during incubation more closely resembled those of fetal plasma than maternal plasma lipids as measured in previous studies. These data are consistent with the view that the equine placenta is a source of both FFA and phospholipid for the fetus and that the placenta may provide long chain polyunsaturated fatty acids for the fetal foal.

Animals↗
PubMedDate not supplied

Differential expression of laminin, nidogen and collagen IV genes in the midgestation mouse placenta.

The distribution of laminin A, B1, B2, nidogen and collagen alpha 1(IV) mRNA was studied in the 12.5-day mouse placenta and uterus. This was compared to the pattern of laminin, nidogen and collagen IV immunoreactivity in the placenta at this time. High levels of B2 mRNA were distributed throughout the decidual layer, compared to lower levels of laminin B1, nidogen and collagen IV. In contrast, laminin B1 and nidogen mRNA were found at very high levels in the trophoblast giant cells and cytotrophoblast. Laminin B2 was much lower in trophoblast cells than in the decidua. Nidogen mRNA levels were low in the decidual cells, but high in endothelial cells lining the placental blood spaces in the decidual layer. Immunofluorescence staining of the placenta showed colocalization of laminin, nidogen and collagen IV in fetal and maternal layers of the placenta. In the antimesometrial area where the uterine epithelium was reforming laminin B1 and B2 mRNA were uniformly distributed between the epithelium and stroma, whereas nidogen and collagen alpha 1(IV) mRNA were only produced by the stromal cells. In all cell types, apart from parietal endoderm cells forming Reichert's membrane, laminin A chain mRNA was very low or absent. These results demonstrate that laminin and nidogen genes are not coordinately expressed in the midgestation mouse placenta. Comparison of the distribution of these mRNAs with collagen alpha 1(IV) mRNA suggests that different regions of the placenta produce specialized extracellular matrices which may contain different ratios of these polypeptides.

Animals↗
PubMedDate not supplied

Short communication: the influence of perfusion in situ on lactate and pyruvate levels in guinea pig placenta.

1. The effect of perfusion in situ on the guinea pig placenta has been investigated using the tissue levels of lactate and pyruvate as biochemical indices. 2. Lactate levels in perfused placentae (10.22 mM) were significantly lower (P less than 0.05) than in non-perfused placentae taken from the same animal, i.e. internal controls (16.39 mM). The concentration of lactate is perfused placentae was similar to that in control placentae taken from animals immediately after induction of Nembutal anaesthesia. 3. It may be concluded that perfusion in situ prevents the significant rise in lactate concentration which is seen in paired-control placentae.

Animals↗
PubMedDate not supplied

Does human placenta produce prostacyclin?

We have previously demonstrated that the human placenta possesses potent platelet anti-aggregatory activity. This activity was exhibited only when aggregation was induced by adenosine diphosphate (ADP), but not when induced by adrenaline, ristocetin or collagen. We have also shown that placental extracts degrade ADP. We therefore concluded that the placenta's anti-aggregatory activity, in vitro, was not due to prostacyclin (PGI2) but to an 'ADPase'. In view of some reports claiming that the human placenta produces PGI2, we carried out a series of experiments to establish whether human placental tissue can convert [14C]-arachidonic acid [( 14C]-AA) to 6-oxo-PGF1 alpha, the stable metabolite of PGI2. Tissue from placenta and the membranes did not show any appreciable conversion of [14C]-AA into 6-oxo-PGF1 alpha. This finding was confirmed by radioimmunoassay techniques where the placenta was shown to produce spontaneously only minimal amounts of 6-oxo-PGF1 alpha. We conclude that placental tissue and the fetal membranes do not synthesize a significant amount of PGI2, certainly not enough to account for the potent platelet anti-aggregatory activity of the placenta in vitro. Placental platelet anti-aggregatory activity in vitro, is probably due entirely to ADPase activity.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Effect of a failure of energy supply on adenine nucleotide breakdown in placentae and other fetal tissues from rat and guinea pig.

The effects of ischaemia on adenylate energy charge of tissues from fetal rats and fetal guinea pigs were measured. Adult rat and guinea-pig tissues, as well as human placentae, were also studied. The largest differences observed were between the fetuses from different pregnant animals (P = 4.74 X 10(-15). Reductions in energy charge in placentae were slower than in other defined fetal tissues, especially brain. In the rat, an immature species at birth, greater 'stability' was observed in placentae of 14 days of gestation than near term at 20 days of gestation. As contrast, in the guinea pig, a mature species at birth, there was no difference in 'stability' in placenta or other fetal tissues between about 40 days of gestation and near term, about 60 days of gestation. In addition to these tissue and maturity effects in the fetus, it has been confirmed that fetal tissues are more 'resistant' than adult tissues to failures of energy supply. Concentrations of adenosine, uridine, guanosine and cytidine nucleotides in placenta show similar patterns in rats and guinea pigs. Fetal liver contains more uridine nucleotides and brain more cytidine nucleotides. It is suggested that the placenta retains an early fetal ability to maintain itself during ischaemia; this might be advantageous during parturition. Possible endocrine and other mechanisms 'damping' fetoplacental metabolism are linked with a discussion of the large maternal effect.

Adenine Nucleotides↗
PubMedDate not supplied

Keratinocyte growth factor and its receptor in the rhesus macaque placenta during the course of gestation.

Keratinocyte growth factor (KGF) is synthesized and secreted exclusively by mesenchymal cells, and acts through its receptor (KGFR) to stimulate epithelial proliferation. In vivo, KGF and KGFR comprise a mesenchymal-epithelial cell paracrine system that can mediate epithelial cell mitosis. In preliminary work, we noted that KGF was expressed in the rhesus monkey placenta, and we now report on the expression of placental KGF and KGFR mRNAs during the course of gestation in this species. In-situ hybridization revealed that during early gestation, KGF mRNA was strongly expressed in placental mesenchymal cells. These cells, which were also immunoreactive for vimentin, were mainly located on the periphery of the mesenchymal cores of both anchoring and floating villi. KGFR mRNA was expressed in the adjacent trophoblastic epithelium, which was immunoreactive for cytokeratin. In-situ hybridization revealed that KGF mRNA expression was very high in the youngest placentae (34-days gestation) and decreased gradually to minimal levels by late gestation (157 days). Northern blot analysis indicated also that the KGF MRNA signal was strongest in early gestation samples and weakest by late gestation. Analysis for KGFR mRNA by a reverse transcriptase-polymerase chain reaction technique showed that KGFR mRNA expression could be detected at all stages. However, in-situ hybridization indicated that KGFR mRNA expression was highest in early gestation placentae and least in the oldest placentae. Autoradiographs of frozen sections of placenta that had been incubated with [125I]KGF to detect receptor binding showed that grain density over the trophoblast was highest in the youngest and least in the oldest placentae. PCNA and Ki-67 expression followed this same temporal trend. We conclude that the KGF/KGFR system may be important in proliferation of the placental trophoblast during early- to mid-pregnancy in rhesus monkeys.

Animals↗
PubMed1996

Maternal-fetal potential difference in the rat is generated by the placenta.

Electrical potential difference, PD, was recorded between maternal blood on one side and uterine lumen (transuterine PD), amniotic fluid (amniotic fluid PD), or vitelline blood of the fetus (maternal-fetal PD) on the other side in rats on day 21 of gestation. The values obtained are 2.4 +/- 6.0 mV (mean +/- s.e.), 11.3 +/- 4.5 mV and 9.6 +/- 4.1 mV, respectively. Maternal-fetal PD recorded over a period of 12 min decreased slowly. It increased transiently when the placenta was separated from the uterus, then it decreased more rapidly than in the corresponding controls afterwards. Maternal-fetal PD did not change significantly when the sac of fetal membranes containing the fetus was exposed intact from the uterus. In other experiments the PD was recorded in vitro between vitelline blood of the fetus which had been removed from the uterus together with intact sac of fetal membranes and a bath of Ringer solution. The PD recorded when only the exposed surface of the placenta (the surface by which the placenta had been attached to the uterus) was immersed in Ringer fluid, was the same as that recorded earlier between maternal and fetal blood in the same fetus. The PD decreased rapidly when the placenta was cooled, and it increased again when the placenta was rewarmed. The PD decreased to near 0 mV when the whole sac of fetal membranes was immersed in Ringer. On the basis of these observations it is concluded that the maternal-fetal PD in the rat is generated by the placenta.

Amniotic Fluid↗
PubMedDate not supplied

Expression of G proteins in human placentae from molar pregnancies.

Hydatidiform mole is a conceptus, usually devoid of an intact fetus, with variable proliferation of trophoblast and altered placental protein synthesis, including high human chorionic gonadotropin (hCG) and low human placental lactogen (hPL) production. Little is known about the control of the production of these two placental proteins in molar pregnancies. Regulatory guanine 5'triphosphate (GTP)-binding proteins (G proteins) play key roles in the endocrine control of peptide production by the placenta. The present authors recently demonstrated that Gi2, Gi3 Go, and Gs alpha-subunits were expressed in normal human placenta throughout pregnancy. This study analysed the expression of placental G protein alpha-subunits in molar pregnancies. Western and Northern blot analyses were performed on membrane protein and total mRNA preparations of human placentae, respectively, from hydatidiform mole (n = 5) and normal pregnancies (n = 4). The levels of hPL and beta-hCG mRNAs were 60 and 237 per cent respectively, of those from normal placentae. The autoradiographs for G proteins and their mRNAs showed decreased expression in molar placentae in comparison with normal tissues. Specifically, G alpha i2, G alpha i3, G alpha o, and G alpha s levels reached 39, 4, 42, and 89 per cent, respectively, of those from normal placentae. In parallel with the protein levels, their mRNAs expression were 8, 3, 54 and 65 per cent of normal values for G alpha i2, G alpha i3, G alpha o, and G alpha s, respectively. The results demonstrate important changes in placental G protein expression in hydatidiform moles suggesting alterations in the signal transduction machinery within the molar trophoblast.

Autoradiography↗
PubMedDate not supplied

Differential distribution of endothelin receptor subtypes in placentae from normal and growth-restricted pregnancies.

The endothelins (ETs) are potent vasoconstrictor peptides that bind to two distinct receptors, ETA and ETB. This study compares the localization of ETA and ETB receptors in placentae complicated by intrauterine growth retardation (IUGR) and abnormal umbilical Doppler waveform, gestationally matched controls, fetuses that were small for gestational age (SGA), and normal term placentae. Quantitative autoradiography was performed using ETA and ETB subtype-selective ligands. Both ETA and ETB receptors were expressed in the human placenta. Gestational and fetal size effects on the receptor density within stem villi were found, but no effect of abnormal placental blood flow could be demonstrated. A distinct spatial distribution of receptor subtypes within the placenta was observed. Smooth muscle cells expressed both receptors with ETA expression predominant in the proximal regions of the villous tree and ETB abundant in the periphery and decidua. Both receptors were also expressed at lower density on paravascular stromal cells in stem villi. Although these data do not demonstrate aberrant localization of ET receptors in IUGR and SGA placentae, the spatially distinct distribution of ET receptors in the human placenta suggests that ETs play a role in modulation of placental blood flow.

Adult↗
PubMedDate not supplied

The ultrastructure of the trophoblastic layer of the degu (Octodon degus) placenta: a re-evaluation of the 'channel problem'.

Previous studies on immersion-fixed specimens of the haemomonochorial labyrinthine chorioallantoic placenta of the degu have made visible channels or pores which completely crossed the trophoblastic layer; for the first time hints for an open connection between maternal blood spaces and fetal interstitium were demonstrated in a placenta. This important finding was re-evaluated by means of transmission electron microscopy paying particular attention to the influence of the mode of fixation and of ischaemic periods prior to fixation. Thirty placentae from seven near-term degu (estimated gestational age 80-90 days) were fixed at various times (5-45 min) after maternal death. Placentae were perfused in situ via the aorta/uterine arteries or the umbilical vein with 2.2 per cent phosphate-buffered glutaraldehyde (n = 7, ischaemic periods < 5-45 min) or lanthanum hydroxide/osmium tetroxide (n = 7, ischaemic periods < 5 min), or were immersion-fixed in 2.2 per cent phosphate-buffered glutaraldehyde (n = 16, ischaemic periods 10-45 min). In material with brief ischaemic periods (n = 3, 5-10 min) no open connections between the maternal blood lacunae and fetal interstitium could be detected. Instead, occasional foci of trophoblast reduced to a thickness of 0.1 micron were found. After ischaemic periods exceeding 10 min, the thin trophoblastic diaphragms had partly disappeared resulting in complete transtrophoblastic pores. It is likely, therefore, that visible trophoblastic pores or channels in the degu placenta are ischaemic artefacts. Application of lanthanum hydroxide from the fetal circulation showed that a branching system of membrane-lined tubules (15-50 nm wide) intruded the trophoblast from its basal side, as has been reported for the guinea-pig and human placenta. It remains to be investigated whether these invaginations belong to a continuous transtrophoblastic channel system.

Animals↗
PubMed1998

Fetal excretion of the fluorescent bile acid derivative cholylglycylamido-fluorescein (FITC-GC) by the rat placenta-maternal liver tandem.

Bile acid transfer from the fetus to maternal bile was studied using in situ perfused rat placenta on day 21 of gestation and a fluorescent derivative of glycocholate (GC): cholylglycylamido-fluorescein (FITC-GC). Single-pass perfusion of the placenta with 0.25 mumol FITC-GC via the umbilical artery over 5 min was followed by the output of 6 per cent of this amount in maternal bile collected over the ensuing 120 min. This amount was reduced (-35 per cent) by simultaneous administration of 2.5 mumol GC through the jugular vein of the mother. This inhibition was stronger (-73 per cent) when 2.5 mumol GC was co-infused with FITC-GC through the umbilical artery. These results suggested that FITC-GC was, at least in part, transported by bile acid carriers across both the liver and the placenta. Using isolated perfused rat livers obtained from female virgin or 21-day pregnant rats, a slight increase in the residence time of FITC-GC in the liver of pregnant rats was found. However, no change in the ability of the liver to take up FITC-GC was observed. By contrast, when FITC-GC was injected into the left jugular vein of anaesthetized pregnant rats, a delayed plasma disappearance of this compound was seen, which may have been due in part to the existence of a transient and reversible FITC-GC exchange with the placental-fetal compartment. The maximal rate of FITC-GC output into bile after FITC-GC administration (1 mumol/100 g body weight) to pregnant rats was approximately 0.2 mumol/min, while maximal FITC-GC bile output was approximately 1 nmol/min when this compound was given through the umbilical artery (2.5 mumol). Therefore, the rate of FITC-GC output into bile was considered to reflect the rate of transfer across the placenta. Using this approach no saturation but rather a linear regression (slope = 1.1 microliters/min, p < 0.05) was found between placental transfer and placental perfusate concentrations in the 10-1000-mumol/l FITC-GC range. In summary, the in situ perfused rat placenta is a useful model to study the fetal excretion of cholephilic compounds, and transfer across the trophoblast would be the limiting step in the excretion of fetal bile acids by the placenta-maternal liver tandem.

Animals↗
PubMed1998

Heme oxygenase and nitric oxide synthase in the placenta of the guinea-pig during gestation.

Nitric oxide (NO) and carbon monoxide (CO) are novel gaseous chemical messengers that play key roles in cell function and cell-cell communication in many organ systems, including the cardiovascular system. Although the presence of NO synthase (NOS) in the placenta and its role in the regulation of fetoplacental and uteroplacental blood flow are well established, little is known about placental expression and activity of heme oxygenase (HO), the enzyme that catalyses the oxidation of heme to CO, biliverdin and iron, during gestation. The objectives of this study were to elucidate the localization of HO-1 and HO-2 isoforms relative to NOS III protein, and to determine the enzymatic activity of HO in the placenta of the guinea-pig during gestation. Placentae were obtained from pregnant guinea-pigs at gestational day (GD) 34, 50, 62 and full term (term, about GD 68). Immunohistochemical localization of HO-1, HO-2 and NOS III protein was conducted using selective polyclonal antibodies. HO activity was determined by using a gas chromatographic method to measure the rate of formation of CO from heme. Faint staining for HO-1 was observed in the adventitial layer of larger fetal blood vessels of the placenta at GD 34. The intensity of this staining was higher at GD 50 and GD 62, and decreased at full term. Similar areas in serial sections of placentae obtained at these selected times during gestation exhibited lower staining intensity when incubated with anti-HO-2 antiserum. Placental HO activity was significantly increased (P<0.05) at GD 62 compared with GD 34, GD 50 and full term. NOS III (endothelial constitutive NOS) staining was highest at GD 34, decreasing thereafter, and was localized mostly to trophoblast lining maternal channels. The data demonstrate that, in the guinea-pig, placental HO and NOS differ in tissue localization during the second half of gestation, with expression of HO protein and its catalytic activity being higher during near-term pregnancy. In a preliminary immunohistochemical investigation of the full-term human placenta, HO-1 protein was localized primarily in the adventitial region of fetal blood vessels of stem chorionic villi. In view of the vasodilator action of CO and NO, the HO and NOS systems may play key roles in the regulation of placental haemodynamics.

Adult↗
PubMed2003

Placental GPI-PLD is of maternal origin and its GPI substrate is absent from placentae of pregnancies associated with pre-eclampsia.

Pre-eclampsia (PE) is a disorder affecting 5-10% of all pregnancies and is characterised by abnormal trophoblast invasion, maternal endothelial cell dysfunction and a systemic maternal response. A unifying factor responsible for eliciting these effects remains unknown. However, levels of the autocrine insulin mediators, inositolphosphoglycans (IPG), are elevated 3-fold in pre-eclamptic placentae compared with controls and are also elevated 3-fold in maternal urine of pre-eclamptic women, suggesting an abnormal paracrine role of the mediator in the systemic maternal response. At the placental level, IPGs are metabolic second messengers capable of eliciting some of the characteristic features of PE, such as the 10-fold increase in glycogen synthesis and 16-fold increase in the activity of the IPG-dependent enzyme glycogen synthase. IPGs are derived from their lipidic precursors, the glycosylphosphatidylinositols (GPI), in membrane associated caveolae by the action of a GPI-specific phospholipase D whose activity is regulated by its membrane microenvironment. We show that the lipidic GPI precursor was detected in total placental membrane and microvillous membrane from normal placentae. The presence of GPI could not be detected in PE placentae, suggesting that the GPI/IPG signalling system is dysregulated in this disorder. Equivalent amounts of a proteolytically-cleaved 50 kDa GPI-PLD protein is detected in both normal and PE placentae. However, GPI-PLD mRNA is absent, suggesting a mechanism of uptake from maternal serum. Since GPI-PLD, whose presence is required for hydrolysis of GPI and release of free IPG, is detectable with equal activity in both normal and PE placentae, we postulate that dysregulation of the tubular caveolar structure of the microvilli in pre-eclamptic placentae provides an environment which promotes the unregulated hydrolysis of GPI in this disorder.

Chorionic Villi↗
PubMed1997

DNA adducts in human placenta as related to air pollution and to GSTM1 genotype.

DNA adducts in human placenta have been studied in relation to metabolic genotype for glutathione S-transferase M1 (GSTM1) in 98 mothers living in two regions with a different annual average air pollution levels: Northern Bohemia-the district of Teplice as polluted industrial area (mines, brown coal power plants) and Southern Bohemia-the district of Prachatice as agricultural area without heavy industry. Forty-nine placenta samples (25 from the Teplice district and 24 from the Prachatice district) from non-smoking mothers with the date of delivery in the summer period and 49 placenta samples (25 from the Teplice district and 24 from Prachatice district) from mothers with the date of delivery in the winter period were analysed. The total DNA adduct levels were calculated as the sum of adducts in the diagnoal radioactive zone (DRZ) and one distinct spot outside of the DRZ (termed X), which was detected in almost all placenta samples. We found total DNA adduct levels of 1.40 +/- 0.87 (0.04-3.65) and 1.04 +/- 0.63 (0.11-3.08) adducts per 10(8) nucleotides for the Teplice and Prachatice districts, respectively. The significant difference between both districts in placental DNA adduct levels was found for the winter sampling period only (1.49 vs. 0.96 adducts per 10(8) nucleotides; p = 0.023). No seasonal variation was observed for DNA adduct levels in the overall population studied. A positive GSTM1 genotype was detected in 51 subjects, while GSTM1-null genotype was found in 47 subjects. Higher DNA adduct levels were detected in a group with GSTM1-null genotype (p = 0.009). This finding seems more significant for subjects in the Teplice district (p = 0.047) than for those in the Prachatice district (p = 0.092). Significant district and seasonal differences were found in subgroups carrying the GSTM1-null genotype. DNA adduct levels in placentas of mothers with GSTM1-null genotype living in the polluted district of Teplice were higher than those in Prachatice (p = 0.050); also the adduct levels in placentas sampled in the summer period were higher than those sampled in the winter period (p = 0.011). Our results indicate that simultaneous analysis of DNA adducts and metabolic genotypes could emphasize the use of DNA adduct measurements, particularly in the case of the environmental exposure when the total doses of genotoxic pollutants are very low.

Adult↗
PubMed2002

Vasoconstrictive activity of oxytocin in meconium impregnated human placentas.

OBJECTIVE: The aim of our study is to determine whether oxytocin acts differently on the fetal-placental vascular bed of normal and meconium impregnated placentas. STUDY DESIGN: Isolated placental cotyledons (n=10) were dually perfused with fetal perfusion pressure used as an index of vascular resistance. As perfusion medium we used lactated Ringer salt solution, containing polyvinylpyrolidone (25 g/l), bovine serum albumin (0.1 mg/ml), glucose (1.0 g/l), heparin (20 IU/ml) and gentamycin (48 microg/ml). The pH of the medium was adjusted to 7.4 with bicarbonate. The maternal site was gassed with 95% O(2):5% CO(2) and in the fetal site with 95% N(2):5% CO(2) at 37 degree C. Perfusion rates were 4-6 and 10-12 ml/min in the fetal and maternal circulation, respectively. TNF-alpha and IL-beta1 levels in the fetal-placental perfusate were evaluated using specific commercial ELISA kits. RESULTS: No significant changes in the amount of TNF-alpha release were observed after injection of oxytocin into the fetal circulation (31+3pg/ml; P=0.5). No IL-beta1 activity was observed in the fetal perfusate of normal and meconium impregnated placentas during the experiments. No significant difference was seen in basal perfusion pressure in normal and meconium impregnated placentas, however, a bolus injection of oxytocin (10U/ml) resulted in a significant increase in perfusion pressure in meconium impregnated placentas from basal pressure of s45+5 to 88+4 mm Hg after injection of oxytocin, (P=0.004, ANOVA). CONCLUSION: Vasoconstrictive effect of oxytocin was observed only in meconium impregnated placentas and no vascular effect of oxytocin was documented in normal placentas. The clinical implication of our findings is that one should use oxytocin for stimulation of labor with caution in the presence of meconium stained amniotic fluid.

Case-Control Studies↗
PubMed2002

Tissue factor (TF) and tissue factor pathway inhibitor (TFPI) in the placenta and myometrium.

BACKGROUND: Placental abruption is mainly due to the rupture of the uterine spiral arteries, but adjacent tissues are also damaged and substances derived from disintegrated placenta and myometrium probably cause coagulation disturbances, such as hypofibrinogenemia and disseminated intravascular coagulation (DIC). AIM: To measure whether placenta and myometrium are significant sources of tissue factor (TF) and tissue factor pathway inhibitor (TFPI), the components of key role in the initiation of coagulation. MATERIALS AND METHODS: Strips of placenta and myometrium were obtained from 48 women delivered by cesarean section at term. TF and TFPI concentrations were measured by immunoenzymatic method (ELISA) in tissue homogenates. MAIN RESULTS: Concentration of TF in placenta and myometrium was 31 (25-37) and 7.4 (4.9-11.4) ng/mg of total protein, respectively. In the plasma of the same women, it was 0.004ng/mg of total protein. TFPI concentration was 13 (10-17) ng/mg of total protein in placenta, 4.5 (3.1-7.3) ng/mg in myometrium, and 0.70 (0.50-0.80) ng/mg in blood plasma protein. CONCLUSION: The levels of TF in placenta and myometrium, over TF in blood plasma may be clinically significant in obstetrics, for instance, in the etiology of DIC in placental abruption. The concentration of TFPI-natural inhibitor of TF-seems to be too low to prevent initiation of coagulation.

Adult↗
PubMed1995

Patterns of bcl-2 expression in placenta.

A total of 39 placentas, whose gestational ages ranged from 8 to 41 weeks, were analyzed for bcl-2 expression using immunohistochemistry and immunoblotting. Immunohistochemically, both intracytoplasmic and nuclear expression of bcl-2 was observed in villous and extravillous trophoblasts, villous mesenchymal cells and capillary endothelial cells, villous macrophages, intermediate trophoblasts, amnionic epithelium, and even in decidua and endometrial glandular epithelium in early gestational periods. The degree of expression significantly decreased in the placentas after the gestational period of 32 weeks which coincides with the declining phase of placental increase. On immunoblotting lysates of 10(4) cells from single cell suspensions of fresh placentas, bcl-2 was detected in the placentas of 22 and 33 gestational weeks, but it was negligible or absent in three term placentas. The results of the present study suggest two possible implications on the role of bcl-2 in placenta: 1) it may be a type of proliferation or maturation-related marker, especially of trophoblasts, which show decreased expression along with terminal differentiation and maturation, and 2) because the primary role of bcl-2 is the inhibition of programmed cell death (PCD), the decrease in placental bcl-2 around term may be a parturition-associated biological change.

Female↗