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At least 19 recordsLinked to original sources
PubMed2005

Circulating placental RNA in maternal plasma is associated with a preponderance of 5' mRNA fragments: implications for noninvasive prenatal diagnosis and monitoring.

BACKGROUND: The molecular characteristics of placental RNA circulating in maternal plasma are unknown. We investigated the integrity of circulating placental RNA in maternal plasma and tested the relevance of plasma RNA integrity for noninvasive prenatal diagnosis. METHODS: Six different placental transcripts and mRNA of the housekeeping gene glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were quantified for the 5' and 3' regions in maternal plasma by 1-step real-time reverse transcription-PCR (RT-PCR) assays. This quantitative strategy was validated by 2-step RT-PCR and serial dilution experiments. The rates of detection by the 5' and 3' assays for the beta-subunit of human chorionic gonadotropin (beta hCG) were assessed in maternal plasma samples collected from different gestational periods. RESULTS: For 5 of the 7 genes, the plasma mRNA concentrations measured by the 5' amplicons were significantly higher than those measured by the corresponding 3' amplicons. Every transcript under study demonstrated a higher rate of detection in the 5' assay than in the 3' assay in maternal plasma. In particular, the detection rate of beta hCG mRNA in maternal plasma was increased throughout gestation when the 5' assay was used. CONCLUSIONS: Circulating placental RNA is associated with a preponderance of 5' mRNA fragments in maternal plasma. Apart from its intrinsic biological interest, this information could have important implications for the development of new assays targeting fetal RNA markers for noninvasive prenatal diagnosis and monitoring.

Chorionic Gonadotropin↗
PubMed1991

Vascular responses of umbilical-placental circulation to vasodilators in fetal lambs.

It has been suggested that the umbilical-placental circulation is maximally vasodilated under normal conditions. To test this hypothesis, we investigated the effect of vasodilators on umbilical-placental vascular resistance. In nine chronically instrumented fetal lambs, catheters were placed in the descending aorta, umbilical artery, umbilical vein, and inferior vena cava. Umbilical-placental blood flow was measured by an electromagnetic flow probe placed around the common umbilical artery. Forskolin and nitroglycerin both dilated the umbilical-placental circulation, causing a dose-dependent decrease in umbilical-placental resistance to approximately 80% of baseline, indicating that the umbilical-placental circulation has some dilatory reserve. Both the adenosine 3',5'-cyclic monophosphate and the guanosine 3',5'-cyclic monophosphate mechanisms, which are directly stimulated by forskolin and nitroglycerin, respectively, are functional in the umbilical-placental circulation. However, the vasodilators prostacyclin and adenosine, which act through specific cell membrane receptors, have no effect on the umbilical-placental resistance. The inability of these agents to dilate the umbilical-placental circulation could be due to a lack of the appropriate receptors in the umbilical-placental vasculature.

Adenosine↗
PubMed1992

Attenuation of the vasoconstrictor effects of thromboxane and endothelin by nitric oxide in the human fetal-placental circulation.

OBJECTIVE: We hypothesized that the endothelial-derived relaxing factor nitric oxide may contribute to low resting vascular tone and may attenuate vasoconstrictor action in the human fetal-placental circulation. STUDY DESIGN: Isolated human placental cotyledons were dually perfused in vitro, and the effects of N-monomethyl-L-arginine and N-nitro-L-arginine (3 x 10(-4) mol/L), which are nonmetabolizable analogs of L-arginine, the substrate for nitric oxide synthase, on resting perfusion pressure and on the fetal-placental circulation preconstricted with U46619 (10(-8) mol/L) or endothelin-1 (10(-8) mol/L) were established. Responses before and after inhibition were compared by paired t test. The effects of glyceryl trinitrate (10(-6) mol/L), acetylcholine (10(-4) mol/L), the calcium ionophore A23187 (10(-6) mol/L), and histamine (10(-8) to 10(-4) mol/L) were also determined in the preconstricted fetal-placental circulation. RESULTS: Both N-monomethyl-L-arginine and N-nitro-L-arginine (3 x 10(-4) mol/L) increased resting perfusion pressure (p less than 0.06), and N-nitro-L-arginine promptly and significantly increased perfusion pressure in the fetal-placental circulation preconstricted with U46619 (p less than 0.0004) or endothelin-1 (p less than 0.06). Nitric oxide generated by addition of glyceryl trinitrate (10(-6) mol/L) attenuated the vasoconstrictor effects of U46619 (p less than 0.026) or endothelin-1 (p less than 0.01). Neither acetylcholine nor the calcium ionophore A23187 had an effect on the fetal-placental circulation, whereas bradykinin further increased perfusion pressure. Histamine only relaxed the preconstricted preparations at concentrations (10(-6) to 10(-4) mol/L) above those shown to release nitric oxide in other systems. CONCLUSION: The stimulus to nitric oxide generation in the fetal-placental circulation may be hydrodynamic. Nitric oxide appears to contribute to maintenance of basal vascular tone and to attenuate the actions of vasoconstrictors in this circulation.

Acetylcholine↗
PubMed2002

Short-term effects of glucocorticoids in the human fetal-placental circulation in vitro.

A number of studies demonstrate that both long-term and short-term exposure to glucocorticoids alters vascular function. We have examined whether the short-term administration of glucocorticoids into the human fetal-placental circulation affects placental arterial pressure and alters vascular responses to vasoconstrictive and vasodilator agents. Single lobules of term human placentae were bilaterally perfused in vitro with Krebs' solution (maternal and fetal, 5 ml/min Krebs, 95% O2, 5% CO2, 37 C, pH 7.3), and changes in fetal-placental arterial perfusion pressure were measured. Dexamethasone (100 nM) infusion for 1 h into the fetal-placental circulation caused a significant decrease in basal arterial pressure (n = 19, t test, P < 0.05). Continuous dexamethasone infusion (100 nM) did not alter vasoconstrictive responses to PGF(2alpha) (0.5-120 pM, n = 12, ANOVA, P > 0.05) or potassium chloride (5-600 mM, n = 12, ANOVA, P > 0.05) or vasodilator responses to CRH (53-7400 pM, n = 13, ANOVA, P > 0.05). However when fetal-placental vessels were submaximally preconstricted and then infused with dexamethasone alone (40 nM-10 microM), there was a dose-dependent decrease in arterial pressure (n = 8). Dexamethasone-induced dilation was not inhibited by blocking nitric oxide synthase or cyclo-oxygenase activity. These data suggest that dexamethasone can cause dilation in the fetal-placental circulation, possibly via an endothelium-independent pathway.

Adult↗
PubMed1991

Investigation of placental circulations by color Doppler ultrasonography.

The placental circulations of 25 normal and five complicated pregnancies were studied by color Doppler ultrasonography. Flow velocity waveforms were obtained in all 30 pregnancies and could discriminate between fetal and maternal intraplacental blood flow. We believe that color Doppler ultrasonography will improve our understanding of the pathophysiology of various pregnancy disorders that alter the placental circulations and that color ultrasonography is useful for the prenatal differential diagnosis of intrauterine masses.

Blood Flow Velocity↗
PubMed1989

[Functional reserve of umbilico-placental circulation].

The authors present the results of the action of 10% magnesium sulphate on the umbilico-placental circulation. They found that intravenous administration of magnesium sulphate reduces the vascular resistance in the umbilico-placental circulation and improves its parameters when a functional disorder is involved. The maximum effect was recorded during the 10th minute following administration. In case of absolute reduction of the placental circulation or in case of an obstruction in the umbilical artery the above parameters did not improve. Magnesium sulphate administration may serve as a loading test of the functional reserve of the umbilico-placental circulation.

Blood Flow Velocity↗
PubMed1997

Vascular effects of PTHrP (1-34) and PTH (1-34) in the human fetal-placental circulation.

The aim of this study was to examine the vasodilatory effects of parathyroid hormone-related protein (PTHrP) (1-34) and parathyroid hormone (PTH) (1-34) on the human fetal-placental circulation utilising an in vitro placental perfusion model. In all experiments, the vasculature of an isolated human placental cotyledon was pre-constricted with the thromboxane A2 mimetic U46619. A simple dose of PTHrP (1-34) or PTH (1-34) (1.7-300 nM) was then infused into the fetal-placental circulation of the cotyledon. In other experiments, cotyledons were repeatedly infused with PTHrP (1-34) or PTH (1-34) (51.3 nM). Vasodilatory responses were significantly reduced in response to repeated exposure to PTHrP (1-34) (P < 0.001), indicating that this peptide desensitizes the fetal-placental vasculature. PTHrP (1-34) and PTH (1-34) equipotently stimulated a significant vasodilation of the fetal-placental circulation (P < 0.0001). The PTHrP receptor antagonist [Asn10, Leu 11]PTHrP (7-34) (102 nM) was infused in U46619-constricted placentae in the presence and absence of PTHrP (1-34) (10.2 nM). The PTHrP antagonist alone had no significant effect in the fetal-placental circulation. The antagonist significantly attenuated the response to PTHrP (1-34) (P < 0.015). Based on the data obtained in this study it is suggested that locally produced PTHrP (1-34) may be involved in the regulation of normal human fetal-placental vascular tone in autocrine and/or paracrine fashion.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1995

Effects of captopril on the human foetal placental circulation: an interaction with bradykinin and angiotensin I.

1. The mechanism underlying the foetal toxicity induced by captopril is not well understood. Since bradykinin and angiotensin II appear to be important in the regulation of the placental circulation, experiments were performed to assess the effects of captopril on the vascular actions of these peptides on the human foetal placental circulation. 2. Full-term human placentas, obtained from normal pregnancy, were perfused with a modified Tyrode solution bubbled with O2 using a pulsatile pump. The placental perfusion pressure was measured with a Statham pressure transducer and recorded continuously on a Hewlett-Packard polygraph. 3. Bradykinin (0.1, 0.3 and 1.0 nmol) injected into the placental arterial circulation produced an increase in placental perfusion pressure in all experiments. This effect of bradykinin was significantly inhibited by indomethacin (3 x 10(-7) M). 4. Captopril (10(-7) M) significantly potentiated the pressor effect of bradykinin on the human placental circulation (n = 6). This effect of captopril was reversed by indomethacin (3 x 10(-7) M). 5. Angiotensin I (n = 6) and angiotensin II (n = 6), injected into the placental arterial circulation, both produced dose-dependent increases in placental perfusion pressure. The dose-response curves to angiotensin I (n = 6) were significantly displaced to the right by captopril in a concentration-dependent manner. 6. We suggest that the toxic effects of captopril on the foetus, rather than reflecting an inhibition of angiotensin II formation, may instead be related to a potentiation of the vasoconstrictor effect of bradykinin on the foetal placental circulation, thereby reducing blood flow and causing foetal damage. The reasons for this are discussed.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed1996

Adrenocorticotropin causes vasodilatation in the human fetal-placental circulation.

During human pregnancy, ACTH is produced by both the placenta and fetal pituitary. ACTH has been shown to cause vasodilatation in the adrenal cortex in vitro. In this context we have investigated the vasoactive effects of ACTH in the human fetal-placental circulation. Single lobules of term human placentas were bilaterally perfused in vitro with Krebs solution (maternal and fetal, 5 mL/min; 95% O2-5% CO2; 37 C; pH 7.3), and changes in fetal placental arterial perfusion pressure (FAP) were measured. ACTH (40-4000 pmol/L; n = 5) caused a dose-dependent reduction of both KC1 and PGF2alpha-induced increases in FAP in the fetal placental circulation. The reductions were of a similar magnitude in the presence of either constrictor agent. ACTH was 187.4 (95% confidence limits, 162.7-215.9) times more potent than prostacyclin (PGI2; 1.2-1180 nmol/L; n = 6), which is a known vasodilator of the fetal-placental circulation. The threshold concentrations for ACTH and PGI2 were 40 pmol/L and 1.2 nmol/L, respectively. ACTH-induced reductions in PGF2alpha-induced increases in FAP in the fetal placental circulation were not inhibited by the nitric oxide synthase inhibitor, N omega-nitro-L-arginine (100 micromol/L; n = 5), the cyclooxygenase inhibitor indomethacin (3 micromol/L; n = 5), or a guanylate cyclase inhibitor LY83583(1 micromol/L; n = 5). The inhibitory effect of ACTH was attenuated by the antagonist, ACTH-(7-38) (240 pmol/L; n = 4), and a polyclonal ACTH antiserum (1:1000 dilution; n = 4). We have demonstrated that ACTH causes a reduction in fetal placental vascular resistance in the human fetal-placental circulation in vitro. The mechanism by which it exerts these effects has not been defined, but neither nitric oxide nor PG-mediated pathways appear to be involved.

Adrenocorticotropic Hormone↗
PubMed1994

The utero-placental circulation, eugenics and the prevention and treatment of high risk pregnancies.

Through systematic experimental and clinical studies, the physiological regulation of utero-placental circulation and the relation of the disturbance in this acirculation to pathogenic mechanisms of high risk pregnancies-Intrauterine Growth Retardation (IUGR) and Pregnancy-induced hypertension (PIH) were explored. The pharmacological effects and mechanism of a Chinese herbal medicine-Qingxintong in improving, the utero-placental circulation and the therapeutic efficacy in treatment of IUGR and PIH, both accompanied by disturbance of utero-placental circulation, were investigated as well.

Acetophenones↗
PubMed1996

Effects of L-arginine on utero-placental circulation in growth-retarded fetuses.

BACKGROUND: To evaluate the effects of L-arginine (ARG) infusion, the nitric oxide as substrate, on the utero-placental circulation at third trimester. METHODS: Three groups of nine pregnant women each were infused i.v. with 30 g ARG, for 30 minutes. One group served as control, and the two remnants were composed by patients with intrauterine growth retardation with (IUGR-B) or without (IUGR-A) increased resistances in the utero-placental circulation. Changes of blood flow velocity waveforms of both uterine arteries and umbilical artery were recorded for 60 minutes. Blood pressure, serum nitrites/nitrates and growth hormone levels were also measured. RESULTS: No hemodynamic changes in utero-umbilical circulation were observed during infusion in any of the three groups. Considering the uterine arteries separately as placental and non-placental sided we found a significant decrease of non-placental side resistances in IUGR-B women. Indeed, the pulsatility index was lowered by 14%, in respect of baseline value. Serum nitrites/nitrates as well as serum growth hormone levels were significantly increased by ARG, in every woman, irrespective of the presence of fetal growth retardation. Blood pressure remained unaffected during infusion in every woman. CONCLUSIONS: These findings suggest that L-arginine infusion affects utero-placental circulation in patients with IUGR associated with increased uterine resistances. Such an action is specific and appears possibly to be mediated by a release of nitric oxide.

Adult↗
PubMed1986

Effect of captopril on bradykinin inactivation by human foetal placental circulation.

The inactivation of bradykinin on passage across the human foetal placental circulation was investigated in six full-term human placentas. The placentas were perfused with a modified Krebs-Henseleit solution and placenta perfusion pressure was recorded. Samples collected at the arterial inflow and at the venous effluent were assayed on the isolated guinea-pig ileum as an estimation of bradykinin activity. Bradykinin (100 ng ml-1) was infused through the foetal placental vessels before and during captopril 4 X 10(-7) M. Bradykinin produced a transient increase in placental vascular resistance that was not potentiated by captopril. Bradykinin activity was completely abolished after passage through the foetal placental circulation, and the inactivation was blocked by captopril. These data suggest that angiotensin I converting enzyme (kininase II) might occur in the foetal placental vessels.

Animals↗
PubMed2001

Effects of nitrovasodilators on the human fetal-placental circulation in vitro.

This study examines the vasorelaxation of isolated human placental chorionic plate arteries and the perfused fetal-placental vasculature, in vitro, to a variety of nitrovasodilator compounds including glyceryl trinitrate (GTN) sodium nitroprusside (SNP), S-nitroso-N-acetylpenicillamine (SNAP), S-nitroso-N-glutathione (SNG) and NaNO(2). The effects of these compounds were also examined under conditions of high (>450 mmHg) and low oxygen (<50 mmHg) tension. In a separate series of experiments the effects of GTN and NaNO(2)were further investigated with addition of the antioxidants cysteine (100 microm), glutathione (100 microm) or superoxide dismutase (SOD) (30 I.U./ml). The order of nitrovasodilator potency, when added directly to isolated fetal vessels was GTN=SNP>SNAP=SNG>NaNO(2). The order under low oxygen tension was similar, GTN=SNP>SNG= SNAP>or=NaNO(2). SNG ( approximately fourfold) and NaNO(2)( approximately 50-fold) were significantly more potent under low oxygen conditions. Cysteine, glutathione and SOD were without effect on GTN induced vasodilatation. However, all three agents significantly enhanced (six- to ninefold) the effects of NaNO(2)under similar conditions. When infused directly into the fetal-placental circulation during in vitro perfusion experiments the order of potency was GTN>SNP>or=SNG>or=SNAP>or=NaNO(2). When the nitrovasodilators were infused indirectly via the maternal intervillous space the order of potency was GTN>or=SNP>or=NaNO(2)>or=SNAP=SNG. Our observations suggest that there are important differences in the action of different classes of nitrovasodilator compounds on the fetal-placental circulation. The changes observed with SNG and NaNO(2)may be influenced by levels of tissue oxygenation.

Adolescent↗
PubMed1992

The comparative effects of big endothelin-1, endothelin-1, and endothelin-3 in the human fetal-placental circulation.

OBJECTIVE: This study compared the effects of big endothelin-1, endothelin-1, and endothelin-3 and whether endothelin-converting enzyme was present in the human fetal-placental circulation. STUDY DESIGN: Single cotyledons of term placentas were dually perfused in vitro, and increases in fetal-placental perfusion pressure to bolus injections of big endothelin-1, endothelin-1, and endothelin-3 (8 x 10(-10) to 1 x 10(-7) mol/L) were recorded. Responses to big endothelin-1 (10(-7) mol/L) were measured in the same placenta before and after perfusion of the fetal-placental circulation with the neutral metalloprotease inhibitor phosphoramidon (10(-5) mol/L), which acts as an endothelin-converting enzyme inhibitor. All experiments were performed in at least five separate placentas. RESULTS: Significant concentration-dependent increases in fetal-placental perfusion pressure were seen with endothelin-1 (p < 0.0005), endothelin-3 (p < 0.0256), and big endothelin-1 (p < 0.0034, analysis of variance). Big endothelin-1 always elicited transient vasodilatation before constriction. Phosphoramidon significantly inhibited the vasoconstrictor effect of big endothelin-1 (p < 0.039, paired t test). CONCLUSION: The three endothelins tested are vasoconstrictors, and endothelin-converting enzyme is present in the fetal-placental circulation.

Blood Circulation↗
PubMedDate not supplied

[New findings about placental circulation using ultrasound].

Introduction of transvaginal color Doppler has enabled precise analysis of placental circulation in early pregnancy. The purpose of this paper is to summarize the current understanding of the anatomy and physiology of the early placental circulation. Study of uteroplacental circulation has demonstrated a progressive decrease of peripheral resistance from large toward small branches during first and early second trimester of pregnancy. Doppler study of umbilical circulation has also shown a significant fall of resistance from umbilical artery to its branches. Analysis of uteroplacental circulation in abnormal early pregnancy has shown differences in comparison with normal values. Using of transvaginal color Doppler in early pregnancy is not successful in prediction of abnormal late pregnancy. Color Doppler is useful in diagnosis of placental and umbilical cord pathology. The duration of pulsed Doppler examination in early pregnancy should be reduced to minimum if we want to avoid excessive heating of embryonic tissue.

Female↗
PubMedDate not supplied

Vasodilator effects of parathyroid hormone, parathyroid hormone-related protein, and calcitonin gene-related peptide in the human fetal-placental circulation.

OBJECTIVE: The purpose of our study was to determine the vasoactivity of calcitonin gene-related peptide (CGRP), parathyroid hormone (PTH), and parathyroid hormone-related protein (PTHrP) in the human fetal-placental circulation in vitro. METHODS: Dually perfused placental cotyledons from term pregnancies were used in this study. RESULTS: Calcitonin gene-related peptide, PTHrP (both 10(-10)-10(-6) mol/L), and PTH (10(-8)-10(-6) mol/L) demonstrated a significant concentration-dependent vasodilator effect (P = .0007, P = .0172, P = .0063, respectively), following preconstriction with a thromboxane mimetic U46619. The CGRP-1 receptor inhibitor CGRP8-37 (10(-6) mol/L) significantly inhibited (P = .0131) the CGRP-induced vasodilator effect, while the nitric oxide synthesis inhibitor n-nitro-l-arginine showed no inhibitory effect. CONCLUSIONS: These results demonstrate the vasodilator effects of CGRP, PTH, and PTHrP in the human fetal-placental circulation. Calcitonin gene-related peptide and PTHrP were of equal potency, and both were approximately 100 times more potent than PTH. This study also suggests the CGRP may exert its vasodilator effect through two classes of receptors in the human placenta and may do so independently of nitric oxide.

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

Corticotropin-releasing hormone-induced vasodilatation in the human fetal placental circulation.

The vasoactive effects of corticotropin-releasing hormone (CRH) in the human fetal-placental circulation in vitro have been investigated. Single lobules of term placentae were bilaterally perfused with constant flows of Krebs' solution (maternal and fetal, 5 ml/min, 95% O2, 5% CO2, 37 degrees C, pH 7.3) and changes in fetal-placental arterial perfusion pressure measured. Effects of human (hCRH) and ovine (oCRH) CRH were examined during submaximal vasoconstriction (100-120 mmHg) of the fetal-placental vasculature induced by prostaglandin F2 alpha (PGF2 alpha), (0.7-2 mumol/L). During infusion of hCRH or oCRH (24-7000 pmol/L) a concentration-dependent vasodilatation was observed. Human CRH and oCRH were equipotent as vasodilator agents (regression analysis; P > 0.05; n = 5). The vasodilator response curves to human and ovine CRH were compared to prostacyclin (PGI2) (1.2-1180 nmol/L). Human and oCRH were 53 times more potent than PGI2 (regression analysis, P < 0.05; n = 5). These results indicate that CRH has powerful vasodilator properties in the human fetal-placental circulation and may play a role in control of placental vascular resistance to blood flow.

Adult↗
PubMed1996

Color Doppler sonographic assessment of placental circulation in the first trimester of normal pregnancy.

Our aim was to study placental circulation during the first trimester of normal pregnancy. For this purpose, 108 single pregnancies from 4 to 15 gestational weeks were evaluated through conventional Doppler ultrasonography. The flow velocity waveforms from the retrochorionic arteries (spiral-radial arteries) and the umbilical artery were assessed using the peak systolic velocity, resistive index, and pulsatility index). Intervillous flow velocity waveform was evaluated from the maximum velocity. The earliest color signal from the retrochorionic circulation was registered at 4.5 weeks along with gestational sac visualization. The venous Doppler signal from the intervillous space and the Doppler signal from the umbilical artery were recorded with an embryo visible from the end of week 5 onward. The retrochorionic, intervillous, and umbilical peak systolic velocities increase, whereas the resistive and pulsatility indices decrease progressively during early pregnancy with a significant correlation with gestational age. Similarly, intervillous maximum velocity gradually increases throughout the first trimester of pregnancy. Despite some methodologic problems related to Doppler technology and the vessels studied color Doppler sonography appears to be an adequate tool to assess the physiologic changes in the placental circulation during early pregnancy.

Blood Flow Velocity↗