Journal articles on the topic 'Placental perfusion'
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1
Mose, Tina, Lisbeth E. Knudsen, Morten Hedegaard, and Gerda K. Mortensen. "Transplacental Transfer of Monomethyl Phthalate and Mono(2-ethylhexyl) Phthalate in a Human Placenta Perfusion System." International Journal of Toxicology 26, no. 3 (May 2007): 221–29. http://dx.doi.org/10.1080/10915810701352721.
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The transplacental passage of monomethylphtalate (mMP) and mono (2-ethylhexyl) phthalate (mEHP) was studied using an ex vivo placental perfusion model with simultaneous perfusion of fetal and maternal circulation in a single cotyledon. Umbilical cord blood and placental tissue collected both before and after perfusion were also analyzed. Placentas were obtained immediately after elective cesarean section and dually perfused in a recirculation system. mMP or mEHP was added to maternal perfusion medium to obtain concentrations at 10 and 25 μg/L, respectively. The placental transfer was followed analyzing samples from fetal and maternal perfusion media by liquid chromatography–mass spectrometry–mass spectrometry (LC-MS-MS). Four perfusions with mMP indicated a slow transplacental transfer, with a fetomaternal ratio (FM ratio) of 0.30 ± 0.03 after 150 min of perfusion. Four perfusions with mEHP indicated a very slow or nonexisting placental transfer. mEHP was only detected in fetal perfusion media from two perfusions, giving rise to FM ratios of 0.088 and 0.20 after 150 min of perfusion. Detectable levels of mMP, mEHP, monoethylphthalate (mEP), and monobutylphthalate were found in tissue. Higher tissue levels of mMP after perfusions with mMP compared to perfusions with mEHP suggest an accumulation of mMP during perfusion. No tendency for accumulation of mEHP was observed during perfusions with mEHP compared to perfusions with mMP. Detectable levels of mEHP and mEP were found in umbilical cord plasma samples. mMP and possibly other short-chained phthalate monoesters in maternal blood can cross the placenta by slow transfer, whereas the results indicate no placental transfer of mEHP. Further studies are recommended.
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Gude, NM, RG King, and SP Brennecke. "Endothelin: release by and potent constrictor effect on the fetal vessels of human perfused placental lobules." Reproduction, Fertility and Development 3, no. 4 (1991): 495. http://dx.doi.org/10.1071/rd9910495.
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Human placental lobules were bilaterally perfused with a modified Krebs solution at constant flow rates of 5 mL min-1, and fetal inflow perfusion pressure was recorded. The effect of infusions of endothelin-1 and endothelin-3 (ET-1 and ET-3) on the perfusion pressure was assessed and compared with that for the thromboxane A2-mimetic U46619 and prostaglandin F2 alpha (PGF2 alpha). All substances caused significant increases in pressure, ET-1 being the most potent, followed in order by U46619, ET-3 and PGF2 alpha. In addition, ET-like immunoreactivity was identified in the fetal effluent of placental lobules during 4 h of basal perfusion. The mean ET-1 equivalent immunoreactivity at 1 h of perfusion was 0.6 +/- 0.2 fmol min-1 g-1 of wet lobule weight for 10 placentae. These data suggest that human fetal placental endothelial cells are capable of synthesizing ETs and that ETs are potent constrictors of the fetal placental vessels. Thus, endothelins may play a role in the control of fetal vascular tone in the human placenta in normal and/or pathological conditions.
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Malek, A., R. K. Miller, D. R. Mattison, T. Ceckler, M. Panigel, P. A. di Sant'Agnese, and L. N. Jessee. "Continuous measurement of ATP by 31P-NMR in term human dually perfused placenta in vitro: response to ischemia." Journal of Applied Physiology 78, no. 5 (May 1, 1995): 1778–86. http://dx.doi.org/10.1152/jappl.1995.78.5.1778.
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ATP was examined in dually perfused term human placentas by using 31P-nuclear magnetic resonance (NMR) spectroscopy. 31P-NMR spectra were acquired every 30 min starting approximately 30 min after establishing fetal and maternal perfusions, and maternal perfusate samples were obtained to monitor glucose utilization, lactate production, and human chorionic gonadotropin (hCG) and human placental lactogen (hPL) release. In continuous-perfusion experiments, placentas were perfused as long as 10 h. ATP increased and Pi fell after initiation of perfusion. Fetal volume loss was < 2 ml/h, and constant production of hCG, hPL, and lactate as well as constant utilization of glucose were observed. In additional experiments, ischemia was produced by halting maternal and fetal perfusion pumps after a 2-h control period. After 2, 3, or 4 h of ischemia, ATP decreased 46 +/- 17, 51 +/- 5, and 85% of control, respectively. When perfusion was reinitiated, ATP increased and was maintained for the duration of the experiment (an additional 2 h). Recovery of ATP after reperfusion was not paralleled by recovery in glucose utilization, lactate production, or hPL and hCG release. However, during the reperfusion period, fetal pressure was < 70 mmHg and fetal volume loss was < 2 ml/h. These investigations suggest that the dually perfused human placental lobule can maintain ATP for > or = 10 h. Although the perfused human placenta recovers ATP and maintains fetal perfusion volume after ischemia lasting up to 4 h, utilization of glucose, production of lactate, and production and release of hCG and hPL are impaired.
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Shaw, A. J., M. Z. Mughal, M. J. Maresh, and C. P. Sibley. "Sodium-dependent magnesium transport across in situ perfused rat placenta." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 2 (August 1, 1991): R369—R372. http://dx.doi.org/10.1152/ajpregu.1991.261.2.r369.
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Placentas of anesthetized rats were perfused in situ on the fetal side to study mechanisms of Mg2+ transport. The perfusate was a Mg(2+)-free Krebs-Ringer, and the unidirectional transfer of Mg2+ from maternal plasma to this Ringer was compared with that of 45Ca and 51Cr-EDTA, the latter being employed as a paracellular diffusional marker. Placental perfusion with amiloride (0.5 mM) or ouabain (1 mM) both rapidly (4 min) reduced maternal-fetal clearance (Kmf) for Mg2+ but had no effect on Kmf for 45Ca. In contrast, perfusion of the carbonic anhydrase inhibitor acetazolamide (1 mM) did not affect Kmf for Mg2+ or 45Ca. Placental perfusion with a Na+-free Ringer reduced Kmf for both Mg2+ and 45Ca, although the latter response was delayed. Kmf for 51Cr-EDTA was increased by amiloride and was unaffected by perfusion of ouabain, acetazolamide, or Na+-free Ringer, indicating that the effects of these treatments on Kmf of Mg2+ do not reflect nonspecific effects on placental permeability. These data suggest that maternal-fetal transfer of Mg2+ across the perfused rat placenta is Na+ dependent.
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Bainbridge, Shannon A., and Graeme N. Smith. "The effect of nicotine on in vitro placental perfusion pressure." Canadian Journal of Physiology and Pharmacology 84, no. 8-9 (September 2006): 953–57. http://dx.doi.org/10.1139/y06-037.
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Cigarette smoking throughout pregnancy is associated with several negative outcomes, of which an increased incidence of intra-uterine growth restriction (IUGR) is most pronounced. Gestationally age-matched infants born to smoking mothers are, on average, 200 g lighter at birth, per pack smoked per day. The mechanisms and specific tobacco compounds responsible for the increased risk of IUGR among smokers have yet to be identified; however, it is widely accepted that smoking women have compromised placental perfusion throughout gestation due to the vasoconstricting effect of nicotine on uterine and placental blood vessels. Despite the universal acceptance of this theory, very little work has been completed to date examining the vasoactive properties of nicotine within the human placenta. The objective of this study was to determine the effect of nicotine on placental vascular function. Normal-term human placentae were obtained after elective cesarean sections. An in vitro placental perfusion system was used; increasing doses of nicotine (20–240 ng/mL) were added to either the maternal (n = 5) or fetal (n = 3) circulation. The basal feto-placental perfusion pressure was 39.87 ± 4.3 mmHg and was not affected by nicotine. This finding supports the hypotheses that nicotine does not directly affect placental microvascular function and that any contribution to fetal growth restriction is likely at the level of placental function (i.e., amino acid transport) and (or) uterine vascular function.
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Lawrence, Dylan J., Kristie Huda, and Carolyn L. Bayer. "Longitudinal characterization of local perfusion of the rat placenta using contrast-enhanced ultrasound imaging." Interface Focus 9, no. 5 (August 16, 2019): 20190024. http://dx.doi.org/10.1098/rsfs.2019.0024.
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The placenta performs many physiological functions critical for development. Insufficient placental perfusion, due to improper vascular remodelling, has been linked to many pregnancy-related diseases. To study longitudinal in vivo placental perfusion, we have implemented a pixel-wise time–intensity curve (TIC) analysis of contrast-enhanced ultrasound (CEUS) images. CEUS images were acquired of pregnant Sprague Dawley rats after bolus injections of gas-filled microbubble contrast agents. Conventionally, perfusion can be quantified using a TIC of contrast enhancement in an averaged region of interest. However, the placenta has a complex structure and flow profile, which is insufficiently described using the conventional technique. In this work, we apply curve fitting in each pixel of the CEUS image series in order to quantify haemodynamic parameters in the placenta and surrounding tissue. The methods quantified an increase in mean placental blood volume and relative blood flow from gestational day (GD) 14 to GD18, while the mean transit time of the microbubbles decreased, demonstrating an overall rise in placental perfusion during gestation. The variance of all three parameters increased during gestation, showing that regional differences in perfusion are observable using the pixel-wise TIC approach. Additionally, the high-resolution parametric images show distinct regions of high blood flow developing during late gestation. The developed methods could be applied to assess placental vascular remodelling during the treatment of the pathologies of pregnancy.
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Hata, Toshiyuki, and Sarah Cajusay-Velasco. "Three-dimensional Power Doppler Ultrasound Study of the Placenta." Donald School Journal of Ultrasound in Obstetrics and Gynecology 8, no. 4 (2014): 400–409. http://dx.doi.org/10.5005/jp-journals-10009-1380.
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ABSTRACT Advanced ultrasound technology has been a valuable tool in the assessment of placental anatomy and physiology. Conventional two-dimensional (2D) sonography reveals placental morphological characteristics, 2D color Doppler can assess blood flow in the placenta, 2D power Doppler can evaluate placental vascular trees, and three-dimensional (3D) ultrasound gives more detailed information on the surface anatomy. Recent advances, such as 3D power Doppler with virtual organ computer aided-analysis (VOCAL) and histogram analysis can measure the placental volume, and assess uteroplacental and fetoplacental perfusions. In particular, ‘placental vascular sonobiopsy’ can specifically evaluate the second- and thirdtrimester placental blood flow and vascularity by obtaining several spherical samples from the placenta that will represent the entire placenta. This article presents normal placental development and pathological findings of the placenta using 3D power Doppler ultrasound, and discusses 3D power Doppler assessments of placental perfusion in high-risk pregnancies, such as fetal growth restriction, pregnancy-induced hypertension and preeclampsia, and, from this basis, re-establishes the importance of 3D power Doppler ultrasound as a screening, diagnostic, and surveillance tool in normal and abnormal pregnancies. How to cite this article Tanaka H, Cajusay-Velasco S, Noguchi J, Hata T. Three-dimensional Power Doppler Ultrasound Study of the Placenta. Donald School J Ultrasound Obstet Gynecol 2014;8(4):400-409.
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Assad, R. S., F. Y. Lee, K. Bergner, and F. L. Hanley. "Extracorporeal circulation in the isolated in situ lamb placenta: hemodynamic characteristics." Journal of Applied Physiology 72, no. 6 (June 1, 1992): 2176–80. http://dx.doi.org/10.1152/jappl.1992.72.6.2176.
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Decreased placental perfusion and respiratory gas exchange have been observed after experimental fetal cardiopulmonary bypass (CPB). To better characterize placental hemodynamics during CPB, seven isolated in situ lamb placentas were placed on a CPB circuit by use of umbilical arterial and venous cannulation. Measures were taken to simulate normal placental hemodynamics. Perfusion flow rates were varied from 15 to 300 ml.min-1.kg fetal wt-1 during normothermia and hypothermia. Placental vascular resistance (PVR) remained constant when perfusion pressure and flow were varied above 40 mmHg and 150 ml.min-1.kg-1, respectively. Below these values, PVR varied inversely. This increase in PVR was more marked when CPB was performed with hypothermia than with normothermia. The clinical implication is that decreased placental flow and pressure on CPB may lead to a vicious cycle, resulting in further impairment of placental perfusion and respiratory gas exchange. Hypothermia promotes this impairment.
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Othoro, Caroline, Julie M. Moore, Kathleen Wannemuehler, Bernard L. Nahlen, Juliana Otieno, Laurence Slutsker, Altaf A. Lal, and Ya Ping Shi. "Evaluation of Various Methods of Maternal Placental Blood Collection for Immunology Studies." Clinical and Vaccine Immunology 13, no. 5 (May 2006): 568–74. http://dx.doi.org/10.1128/cvi.13.5.568-574.2006.
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ABSTRACT The collection of maternal placental intervillous blood (IVB), without contamination of fetal blood and with an accurate mononuclear cell profile, is essential for immunological studies of placental malaria and other infectious diseases of the placenta. We have compared five documented methods of IVB collection: perfusion, incision, biopsy, tissue grinding, and puncture (prick) for fetal blood contamination and mononuclear cell profiles using flow cytometry. Twenty-five placentas were obtained from Plasmodium falciparum and human immunodeficiency virus-negative primigravid and secundigravid women delivering at Nyanza Provincial Hospital in Kisumu, western Kenya. Each of the five methods was performed on the same placenta. Fetal red blood cell contamination was significantly lower for the prick and perfusion methods (4.1% and 8.3%, respectively) than for incision (59.5%), biopsy (42.6%), and tissue grinding (19.9%). Significant variation was noted among the five methods in the percentages of monocytes, total T cells, CD4+ and CD8+ T cells, B cells, and NK cells. Further, a pairwise comparison of prick and perfusion, the two methods with low fetal blood contamination, showed that they were not different for fetal red blood cell contamination levels; however, prick yielded significantly higher percentages of CD4 T cells and CD4 memory T cells than perfusion. Collection by prick was determined to be the best method of intervillous blood collection for immunology studies, and perfusion represented the next best method of choice due to high sample volume yield. Overall, in considering the advantages/disadvantages of the two methods with low fetal cell contamination, we conclude that a combination of prick and perfusion is most suitable for immunology studies.
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Rodda, C. P., M. Kubota, J. A. Heath, P. R. Ebeling, J. M. Moseley, A. D. Care, I. W. Caple, and T. J. Martin. "Evidence for a novel parathyroid hormone-related protein in fetal lamb parathyroid glands and sheep placenta: comparisons with a similar protein implicated in humoral hypercalcaemia of malignancy." Journal of Endocrinology 117, no. 2 (May 1988): 261–71. http://dx.doi.org/10.1677/joe.0.1170261.
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ABSTRACT Parathyroid hormone (PTH)-like bioactivity, assayed as adenylate cyclase response in UMR 106-01 osteogenic sarcoma cells, was present in extracts of sheep fetal and maternal parathyroid glands and placenta. Preincubation of extracts with PTH(1–34) antiserum inhibited approximately 40% of the bioactivity in fetal parathyroid extracts, 50% in maternal parathyroid extracts, but only 10% of the bioactivity in the placental extract. Partial purification of placental extracts by chromatography yielded fractions containing PTH-like bioactivity which were similar in behaviour to that of PTH-related protein (PTHrP) from a human lung cancer cell line (BEN). An antiserum against synthetic PTHrP(1–16) partially inhibited the bioactivity of the placental extract and synthetic PTHrP(1–34), but had no effect on the bioactivity of bovine PTH(1–34) or bovine PTH(1– 84). The placental PTH-like bioactivity was higher in mid- than in late gestation. Fetal parathyroid glands contained the highest PTH-like bioactivity. Thyroparathyroidectomy of one fetal twin lamb in each of 16 ewes between 110 and 125 days of gestation resulted in decreases of the plasma calcium concentration and reversal of the placental calcium gradient that existed between the ewe and the intact fetus. Perfusion of the placenta of each twin in anaesthetized ewes was carried out sequentially with autologous fetal blood in the absence of the exsanguinated fetus. The plasma calcium concentration in the blood perfusing the placenta of each twin increased, but reached a plateau at a lower concentration in the perfusing blood of thyroparathyroidectomized fetuses than in that of the intact fetuses. Addition of extracts of fetal parathyroid glands or of partially purified PTHrP resulted in further increases in plasma calcium in the autologous blood perfusing the placentae of thyroparathyroidectomized fetuses, but addition of bovine PTH(1–84) or rat PTH(1–34) had no effect. The presence of this PTH-like protein in the fetal parathyroid gland and placenta may contribute to the relative hypercalcaemia of the fetal lamb. This protein, which is similar to PTHrP associated with humoral hypercalcaemia of malignancy, stimulates the placental calcium pump responsible for maintaining a relative fetal hypercalcaemia during gestation. J. Endocr. (1988) 117, 261–271
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Hiremath, Jayashree N., and Ramesh P. "Cross-Sectional Study of Placental Surface Area and Umbilical Cord Attachment on Placenta in Normal and PIH Pregnancy and Its Effects on Foetal Weight." International Journal of Anatomy and Research 10, no. 1 (January 5, 2022): 8297–300. http://dx.doi.org/10.16965/ijar.2021.212.
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Introduction: Pregnancy-induced hypertension (PIH) is one of the risk factor in pregnancy leading to placental insufficiency which in turn is responsible for maternal and foetal morbidity and mortality. PIH causes morphological changes in placenta. Decreased placental surface area and variation in the attachment of umbilical cord on placenta are more commonly noted in PIH which hampers the uteroplacental perfusion resulting in foetal mortality and morbidity. Hence afforts were made to study the incidence of reduced placental surface area and mode of cord attachment on placenta. Materials and methods: The study was conducted in the Department of Anatomy, Sri Siddhartha medical college and Hospital, Tumakuru, Karnataka. A total of 100 (50 normal and 50 PIH) human placentae were studied. Placental surface area and mode of attachment of umbilical cord in normal and PIH pregnancy were measured and noted. This study was analysed statistically by using Unpaired t-test and Chi-square test. Results: The study revealed significantly decrease in placental surface area and also there is increased incidence of central and marginal attachment of umbilical cord in PIH cases. Conclusion: Study reveals, PIH cause morphological changes in placenta, it decreasing the uteroplacental blood flow which reduces foetal nutrition ultimately decreasing the neonatal weight. KEY WORDS: PIH, uteroplacental blood flow, neonatal weight, placental surface area and Umbilical cord.
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Langerak, Thomas, Michelle Broekhuizen, Peter-Paul Alexander Unger, Lunbo Tan, Marion Koopmans, Eric van Gorp, A. H. Jan Danser, and Barry Rockx. "Transplacental Zika virus transmission in ex vivo perfused human placentas." PLOS Neglected Tropical Diseases 16, no. 4 (April 20, 2022): e0010359. http://dx.doi.org/10.1371/journal.pntd.0010359.
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A Zika virus (ZIKV) infection during pregnancy can result in severe birth defects such as microcephaly. To date, it is incompletely understood how ZIKV can cross the human placenta. Furthermore, results from studies in pregnant mice and non-human primates are conflicting regarding the role of cross-reactive dengue virus (DENV) antibodies on transplacental ZIKV transmission. Elucidating how ZIKV can cross the placenta and which risk factors contribute to this is important for risk assessment and for potential intervention strategies for transplacental ZIKV transmission. In this study we use an ex vivo human placental perfusion model to study transplacental ZIKV transmission and the effect that cross-reactive DENV antibodies have on this transmission. By using this model, we demonstrate that DENV antibodies significantly increase ZIKV uptake in perfused human placentas and that this increased uptake is neonatal Fc-receptor-dependent. Furthermore, we show that cross-reactive DENV antibodies enhance ZIKV infection in term human placental explants and in primary fetal macrophages but not in primary trophoblasts. Our data supports the hypothesis that presence of cross-reactive DENV antibodies could be an important risk factor for transplacental ZIKV transmission. Furthermore, we demonstrate that the ex vivo placental perfusion model is a relevant and animal friendly model to study transplacental pathogen transmission.
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Yougbare, Issaka, Tai Wei-she, Darko Zdravic, Pingguo Chen, Guangheng Zhu, Howard Leong-Poi, Qu Dawei, et al. "Natural Killer Cells Contribute to Pathophysiology of Placenta Leading to Miscarriage in Fetal and Neonatal Alloimmune Thrombocytopenia." Blood 126, no. 23 (December 3, 2015): 2254. http://dx.doi.org/10.1182/blood.v126.23.2254.2254.
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Abstract Background: Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is a life threatening disease often leading to severe bleeding diatheses, and/or miscarriage; although the incidence of miscarriage has not been adequately studied. FNAIT is caused by a maternal immune response against fetal platelet antigens, in which >80% reported cases have antibodies against β3 integrin. Maternal antibodies and Natural Killer (NK) cells may target antigen positive trophoblast cells and cause miscarriage, but this hypothesis has never been explored.In this study, we investigated whether platelet antibodies and NK cells impaired trophoblast invasion, and placental angiogenesis and function. Methods: β3 integrin deficient female mice were immunized with wild-type (WT) platelets and bred with WT males. Placental vascularisation and function were investigated by echography and micro-computered tomography (CT). Angiogenic and inflammatory cytokines, placenta growth factor (PlGF) and fms-like tyrosine receptor levels (Flt-1) were detected by ELISA. Placental function such as nutrient transport was detected by maternal intravenous administration of biotin and its perfusion to the fetus. NK cell phenotype was assessed by FACS. Placenta pathology was investigated by hematoxylin & eosin staining and immuno-histochemistry for cytokeratin-7, NK cell perforin and smooth muscle actin. Apoptosis and decidual remodeling were investigated by TUNEL assays. In vitro, NK cells were co-cultured with trophoblast cell lines and cytotoxicity was detected by flow cytometry. Results and discussion: Growth restriction and fetal loss/miscarriage only occurred in immunized mothers around embryo day E14.5. Placenta of affected fetuses had significantly reduced vascularization and materno-placental perfusion as demonstrated by ultrasound. CT scan also confirmed shallow development of placental sponge capillaries. These observations are validated by significantly reduced biotin perfusion to the fetuses which had a high hypoxia level. Immunized mice exhibited enlarged spleens as well as an increased Th1 and Th17 immune responses. These pro-inflammatory responses may contribute to trophoblast Flt-1 over-expression and a decreased plasma PlGF/sFlt-1 ratio. E.14.5, the end of organogenesis, is concomitant with trophoblast invasion into spiral arteries. The remodeling of spiral arteries lowers maternal vascular resistance and increases utero-placental blood flow which is critical for healthy pregnancy. Expression of trophoblast marker, Cytokeratin 7, was decreased in the placentas of immunized mice, suggesting scanty invasion invasion. Histology of affected placenta confirmed ischemic tissues, as revealed by significantly reduced numbers of maternal red blood cells in the labyrinth. Unexpectedly, decidual NK cell number remained elevated by day E14.5 in the placenta of immunized mice. Importantly activated NK cells released significant amount of perforin in the placenta, which may destroy target cells expressing β3 integrin. These observations support an abnormal remodeling process mediated by maternal antibodies and NK cells, since increased apoptosis was found in the decidua of immunized pregnant mice compared to naive control. Interestingly, maternal intravenous immunoglobulin therapy ameliorated survival of FNAIT fetuses.. To investigate the molecular and cellular mechanism involved, human choriocarcinoma cells (BeWo) were incubated with both murine anti-β3 antibodies and human HPA-1a IgG. Our data demonstrated, for the first time, that anti-platelet antibodies induced over-expression of the anti-angiogenic molecule, Flt-1 by BeWo cells. Conclusion: Our data suggest that maternal β3 integrin antibodies and NK cells impaired placental pro-angiogenic signalling and function. Reduced trophoblast invasion may cause poor materno-placental perfusion and fetus loss/miscarriage in FNAIT. Disclosures No relevant conflicts of interest to declare.
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Read, MA, WB Giles, IM Leitch, AL Boura, and WA Walters. "Vascular responses to sodium nitroprusside in the human fetal-placental circulation." Reproduction, Fertility and Development 7, no. 6 (1995): 1557. http://dx.doi.org/10.1071/rd9951557.
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This study examined the activity of sodium nitroprusside (SNP) in the human fetal-placental circulation in vitro in pathological and experimental conditions in which vascular function may be impaired. SNP (13-3400 nM) caused a concentration-dependent reduction in fetal arterial perfusion pressure (FAP) in Krebs' perfused placental cotyledons, at basal tone and following pre-constriction with prostaglandin F2 alpha (PGF2 alpha). SNP-induced reduction in FAP in the PGF2 alpha pre-constricted fetal-placental circulation was enhanced approximately six-fold (5.85) in those placentae pre-treated with the nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine (100 microM). Reductions in FAP in the preconstricted fetal-placental vasculature caused by SNP were not altered by prior infusion of ouabain (100 nM) into the fetal circulation or during low oxygen perfusion (O2 tension < 50 mmHg). No differences were observed in the responses obtained to SNP in placentae obtained from women with normotensive pregnancies or those associated with (i) pregnancy-induced hypertension, (ii) intra-uterine growth retardation, or (iii) an elevated umbilical-artery Doppler-ultrasound systolic/diastolic ratio, in either preconstricted placentae or those at basal tone. These findings are consistent with an up-regulation of guanylate cyclase/cGMP-mediated vasodilatation in the fetal-placental vasculature following complete blockade of endogenous NO production.
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Kidima, Winifrida B., Gatambwa D. Mukandala, Osiana Leonard, and Daniel Nkungu. "Placental Insulin-Like Growth Factor-1 Receptor, Protein Kinase B and Mammalian Target of Rapamycin are Downregulated in HIV-1 Positive Women on Antiretroviral Drugs." Tanzania Journal of Science 47, no. 5 (December 1, 2021): 1675–88. http://dx.doi.org/10.4314/tjs.v47i5.16.
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HIV-1 and ARV drugs uptake during pregnancy may change placental phenotype during pregnancy affecting fetal growth. We investigated the influence of maternal HIV-1 and ARV drugs on expression of placental genes important for fetus growth. A total 51 HIV-1 positives and 46 HIV-1 negative pregnant women were studied. Placental gene expression changes of insulin-like growth factor receptor 1 (IGF-1) R, mammalian target of rapamycin (mTOR), protein kinase B (AKT-1), sodium-coupled neutral amino acid transporters (Slc38a1, Slca38a2, Slc38a4), inhibin A, adrenomedullin and 11 beta-Hydroxysteroid dehydrogenase type (HSD)-2 were assessed by RT-qPCR. There was a significant decrease in mRNA expression of placental IGF-1R, mTOR, and AKT-1 in HIV-1 positive placentas compared to controls (p < 0.0001). There was also significant upregulation of an antiangiogenic molecule, inhibin A and downregulation of angiogenic molecule adrenomedullin in HIV-1 positive placenta (all p < 0.0001). However, the mRNA expression of placental Slc38a1 and Slca38a2 was higher in both HIV-1 positive and negative women delivering LBW babies compared to controls (p < 0.0001). The placental mRNA expression of 11 β-HSD-2 increased by 17 folds in HIV-1 negative and by 3.8 folds in HIV-1 positive women delivering LBW babies. IGF-1-P13-AKT-1-mTOR signaling pathway is dysregulated in placenta of HIV-1 positive women on ARV drugs. Higher mRNA expression levels of inhibin A and lower levels of adrenomedullin occur in placenta of HIV-1 positive women delivering LBW babies. ARV drugs and HIV-1 may be involved in the disruption of vascular tone of the placenta and therefore placental perfusion.
Keywords: Pregnant women, HIV-1, ARV drugs, Placental IGF-1-AKT-1-mTOR signaling, inhibin A, adrenomedullin, amino acid transporters.
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Plitman Mayo, Romina, Yassen Abbas, D. Stephen Charnock-Jones, Graham J. Burton, and Gil Marom. "Three-dimensional morphological analysis of placental terminal villi." Interface Focus 9, no. 5 (August 16, 2019): 20190037. http://dx.doi.org/10.1098/rsfs.2019.0037.
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Transport of nutrients and waste between the maternal and fetal circulations during pregnancy takes place at the final branches of the placental villous trees. Therefore, and unsurprisingly, pregnancy complications have been related to the maldevelopment of terminal villi. However, a deep analysis of placental villous morphology has been limited by tissue processing and imaging techniques. In this proof-of-principle study, placental lobules were fixed by perfusion and small clumps of villi were stained, sectioned optically and reconstructed. Morphological and network analyses were suggested and demonstrated on samples of normal placentas. The results show that most parameters are almost constant within a placenta but that there exists an inter-individual variation. Network analysis suggests that the feto-placental capillary network has several paths within an individual villus, serving as an efficient transport system. Three-dimensional reconstruction from confocal laser scanning microscopy images is a potent technique able to quantify placental architecture and capture the significant irregularities in vessel diameter and membrane thickness. This approach has the potential to become a powerful tool to further our understanding of the differences in placental structure which may underlie pregnancy complications.
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Wu, Sing-yung, Charles H. Emerson, Edward Tjioe, and Dong-bao Chen. "Maternal 3,3’-Diiodothyronine Sulfate Formation from Guinea Pig Placenta Perfused with 3,3’,5-Triodothyronine." Endocrinology and Disorders 5, no. 7 (October 25, 2021): 01–06. http://dx.doi.org/10.31579/2640-1045/101.
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Objective: Serum 3, 3’,5-triiodothyronine (T3) remains low in near-term fetus to prevent the growing fetus from undue exposure to its active catabolic effect in mammals. The present study was undertaken to gain insight in the role of placenta in T3 metabolism, fetal to maternal transfer of T3, and its metabolites by in situ placenta perfusion with outer-ring labeled [125I]-T3 in pregnant guinea pig, a species showing increased sulfated 3, 3’-diiodothyronine (T2S) levels in maternal serum in late pregnancy (term = 65 days), similarly to humans in pregnancy. Materials and Methods: One-pass placenta perfusions performed on pregnant guinea pigs were studied between 58 - 65 days of gestation. In two separate experiments, the umbilical artery of the guinea pig placenta was perfused in situ at 37°C with outer-ring labeled [125I]-T3. Maternal sera and umbilical effluents were obtained for analysis at the end of a 60-minute perfusion, when the steady-state levels of radioactivity were reached in the placenta effluent after 30-minute. Results: Sulfated [125I]-T2S was readily detected in the maternal serum as the major metabolite of T3 following the perfusion of placenta with [125I]-T3, suggesting that placental inner-ring deiodinase and sulfotransferase may play an important role in fetal T3 homeostasis and in the fetal to maternal transfer of sulfated iodothyronine metabolites. Conclusions: The expression of type 3 deiodinase (D3) and thyroid hormone sulfotransferase activity in placenta may play an important role to protect developing organs against undue exposure to active thyroid hormone in late gestation in the fetus. The combined activities of D3 and sulfotransferase promoted a placental transfer of T2S into maternal circulation. The maternal circulation of T2S is fetal T3 in origin and its role as a fetal thyroid function biomarker deserves further evaluations and studies.
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Rahi, M., T. Heikkinen, J. Hakkola, K. Hakala, O. Wallerman, M. Wadelius, C. Wadelius, and K. Laine. "Influence of adenosine triphosphate and ABCB1 (MDR1) genotype on the P-glycoprotein-dependent transfer of saquinavir in the dually perfused human placenta." Human & Experimental Toxicology 27, no. 1 (January 2008): 65–71. http://dx.doi.org/10.1177/0960327108088971.
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Background: The ATP-dependent drug-efflux pump, P-glycoprotein (P-gp) encoded by ABCB1 (MDR1), plays a crucial role in several tissues forming blood–tissue barriers. Absence of a normally functioning P-gp can lead to a highly increased tissue penetration of a number of clinically important drugs. Methods: We have studied the dose–response effect of exogenous ATP on the placental transfer of the well-established P-gp substrate saquinavir in 17 dually perfused human term placentas. We have also studied the influence of the ABCB1 polymorphisms 2677G>T/A and 3435C>T on placental P-gp expression ( n = 44) and the transfer ( n = 16) of saquinavir. Results: The present results indicate that the addition of exogenous ATP to the perfusion medium does not affect the function of P-gp as measured by saquinavir transfer across the human placenta. The variant allele 3435T was associated with significantly higher placental P-gp expression than the wild-type alleles. However, neither polymorphism affected placental transfer of saquinavir nor there was any correlation between P-gp expression and saquinavir transfer. Conclusions: Our results indicate that addition of exogenous ATP is not required for ATP-dependent transporter function in a dually perfused human placenta. Although the ABCB1 polymorphism 3435C>T altered the expression levels of P-gp in the human placenta, this did not have any consequences on P-gp–mediated placental transfer of saquinavir.
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Gorkem, Sureyya Burcu, Mehmet Serdar Kutuk, Selim Doganay, Tamer Gunes, Karamehmet Yildiz, and Mustafa Kucukaydin. "Decreased Brain and Placental Perfusion in Omphalopagus Conjoined Twins on Fetal MRI." Radiology Research and Practice 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/9458540.
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The aim of this study is to evaluate perfusional changes in brain and placenta of omphalopagus conjoined twins and to compare them with singleton fetuses by using diffusion weighted imaging and apparent diffusion coefficient. Fetal MRIs of 28-week-old omphalopagus conjoined twins with a shared liver with two separate gallbladders and portal and hepatic venous systems and three singleton fetuses with unilateral borderline ventriculomegaly at the same gestational week as control group were enrolled retrospectively. There was a significant decrease in ADC values of brain regions (p=0.018) and placenta (p=0.005) of conjoined twins compared to the control group. The decreased ADC values in placenta and brain regions in conjoined twins might be due to decreased placental perfusion compared to singleton pregnancy. Our results would be a keystone for future studies which will compare larger group of monochorionic multiple pregnancies with singleton pregnancies.
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BURTON, GRAHAM J., and TAI-HO HUNG. "HYPOXIA-REOXYGENATION; A POTENTIAL SOURCE OF PLACENTAL OXIDATIVE STRESS IN NORMAL PREGNANCY AND PREECLAMPSIA." Fetal and Maternal Medicine Review 14, no. 2 (May 2003): 97–117. http://dx.doi.org/10.1017/s0965539503001049.
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It is now over half a century since Arthur Hertig first reported vascular pathology in the uterine arteries supplying the placenta in women suffering from preeclampsia. His pioneering histological studies have been validated and extended by many others, leading to the general concept that placental perfusion is compromised in these patients. More recent Doppler ultrasound studies have confirmed reduced intervillous blood flow in vivo, and so gradually a consensus has emerged that the placental lesions associated with preeclampsia arise from a state of chronic hypoxia. Whilst hypoxia may undoubtedly play a significant role in the generation of placental pathology, there is considerable evidence that another feature of the intervillous circulation, namely the constancy of the blood flow, may be a more important factor. In this review we propose that hypoxia-reoxygenation, secondary to intermittent perfusion of the intervillous space, is a more physiological approach to take to understanding the pathophysiology of both normal pregnancies, and those complicated by preeclampsia. We further propose that chronic reduction in placental perfusion alone may lead to fetal growth restriction, and that if the two phenomena are superimposed then preeclampsia with growth restriction will result.
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Fokina, Valentina, Svetlana Patrikeeva, Xiaoming Wang, Mansi Shah, Poonam Shah, William K. Russell, Mahmoud S. Ahmed, Erik Rytting, and Tatiana Nanovskaya. "Physicochemical and Biological Properties of Membrane Vesicles Derived from Human Term Placentas." Journal of Biomedical Nanotechnology 18, no. 2 (February 1, 2022): 589–99. http://dx.doi.org/10.1166/jbn.2022.3255.
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The purpose of this study was to conduct initial characterization of membrane vesicles isolated from human placenta by agitation of villous tissue (apical and basal) as well as vesicles obtained following dual perfusion of placental lobule. The morphology, physical and biological properties of the isolated vesicles were determined by electron microscopy, dynamic light scattering, and immunoblotting as well as nanoflow liquid chromatography-mass spectrometry proteomics analysis. CD-1 male mice were used to test the biocompatibility of the vesicles in vivo and assess the biodistribution of fluorescently labeled apical and perfusion vesicles. The vesicles obtained following placental perfusion and the apical vesicles had Z-average diameters of 199±23 nm and 246±24 nm, respectively, and demonstrated nanocarrier stability, low toxicity, and low immunogenicity. On the other hand, administration of basal vesicles resulted in animal demise with LD50 of 0.85 μgprotein/g. Both fluorescently labeled apical and perfusion vesicles were detected in the lungs, liver, kidneys, and spleen of CD-1 mice within 24 h of administration. However, there were differences in organ distribution of these vesicles over 24 hours time period. These data suggest that placental apical and perfusion vesicles have a potential for further development as biological vehicles for drug delivery.
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Gordon, Zoya, Osnat Eytan, Ariel J. Jaffa, and David Elad. "Hemodynamic analysis of Hyrtl anastomosis in human placenta." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 2 (February 2007): R977—R982. http://dx.doi.org/10.1152/ajpregu.00410.2006.
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The Hyrtl anastomosis is a common connection between the umbilical arteries near the cord insertion in most human placentas. It has been speculated that it equalizes the blood pressure between the territories supplied by the umbilical arteries. However, its functional role in the regulation and distribution of fetal blood flow to the placenta has not yet been explored. A computational model has been developed for quantitative analysis of hemodynamic characteristic of the Hyrtl anastomosis in cases of discordant blood flow in the umbilical arteries. Simulations were performed for cases of either increased placental resistance at the downstream end or reduced arterial blood flow due to some pathologies upstream of one of the arteries. The results indicate that when placental territories of one artery impose increased resistance to fetal blood flow, the Hyrtl anastomosis redistributes the blood flow into the second artery to reduce the large pressure gradients that are developed in the affected artery. When one of the arteries conducts a smaller blood flow into the placenta and a relatively smaller pressure gradient is developed, the Hyrtl anastomosis rebuilds the pressure gradients in the affected artery and redistributes blood flow from the unaffected artery to the affected one to improve placental perfusion. In conclusion, the Hyrtl anastomosis plays the role of either a safety valve or a pressure stabilizer between the umbilical arteries at the placental insertion.
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Khan, Nahid Ahmed, Nuzaira Nahid, Melia Choudhury, Khaleda Islam, and Shafinaz Mehzabin. "Morphological study of placenta in selected normotensive and pre-eclamptic women in Bangladesh." Journal of Dhaka Medical College 29, no. 2 (January 10, 2021): 171–77. http://dx.doi.org/10.3329/jdmc.v29i2.51299.
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Pre – Eclampsia is a disorder of 2nd half of pregnancy, which is characterized by a combination of hypertension, proteinuria and edema, secondary to decreased placental perfusion. Clinical studies suggest that there are morphological changes in the placenta of pre-eclamptic women, compared to normotensive pregnant women. In developing countries, pre-eclampsia causes an estimated 50,000 maternal deaths per year. Only a small number of studies have however, been conducted in Bangladesh.
Objective: To compare the morphology of placenta in selected pre-eclamptic and normotensive pregnant women.
Methods: 220 pregnant women were selected with inclusion and exclusion criteria from 3 different medical colleges and divided into 2 groups – A study group, consisting of 110 pre-eclamptic women and a control group consisting of 110 normotensive pregnant women. Dietary information was collected by 7 days food frequency questionnaire and food score was determined. Anthropometric and biochemical tests were performed. To measure the weight of the placentas, the decidual part of the placentas were removed. The umbilical cords were then cut, nearest to the placenta, to drain the blood from the placental vessels, and the weight was recorded upto nearest gram with weighing machine. The diameters of placentas were measured by taking the average of two maximum diameters of placentas with measuring tape (cm).The cotyledons were counted from maternal side after removal of deciduas basalis. Number of placental infarcts were counted from fetal side.
Results: The mean weights, diameters, number of cotyledons were found to be significantly lower in the study group, compared to the control group. The number of infarcted areas was significantly higher in the placentas of pre-eclamptic women
Conclusion: Therefore, weight, diameter and number of cotyledons are decreased and number of infarcted areas are increased in the placenta of pre-eclamptic women, compared to normotensive pregnant women.
J Dhaka Medical College, Vol. 29, No.2, October, 2020, Page 171-177
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Yang, Yike, Huili Jin, Yuhan Qiu, Yamin Liu, Li Wen, Yong Fu, Hongbo Qi, Philip N. Baker, and Chao Tong. "Reactive Oxygen Species are Essential for Placental Angiogenesis During Early Gestation." Oxidative Medicine and Cellular Longevity 2022 (June 1, 2022): 1–14. http://dx.doi.org/10.1155/2022/4290922.
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Background. Preeclampsia (PE) is associated with insufficient placental perfusion attributed to maldevelopment of the placental vasculature. Reactive oxygen species (ROS) are implicated in angiogenesis, but their regulatory effects and mechanisms in placental vascular development remain unclear. Methods. Placental oxidative stress was determined throughout gestation by measuring 4-hydroxynonenal (4HNE) and malondialdehyde (MDA). The antioxidant MitoQ was administered to pregnant mice from GDs 7.5 to 11.5; placental morphology and angiogenesis pathways were examined on GDs 11.5 and 18.5. Moreover, we established a mouse mFlt-1-induced PE model and assessed blood pressure, urine protein levels, and placental vascular development on GDs 11.5 and 18.5. Human umbilical vein endothelial cells (HUVECs) were treated with various H2O2 concentrations to evaluate cell viability, intracellular ROS levels, and tube formation capability. MitoQ, an AKT inhibitor and an ERK1/2 inhibitor were applied to validate the ROS-mediated mechanism regulating placental angiogenesis. Results. First-trimester placentas presented significantly higher MDA and 4HNE levels. MitoQ significantly reduced the blood vessel density and angiogenesis pathway activity in the placenta on GDs 11.5 and 18.5. Serum sFlt-1 levels were elevated, and we observed poor placental angiogenesis and PE-like symptoms in cases with mFlt-1 overexpression. Moderate H2O2 treatment promoted HUVEC proliferation and angiogenesis, whereas these improvements were abolished by MitoQ, AKT inhibitor, or ERK1/2 inhibitor treatment. Conclusions. Moderate ROS levels are essential for placental angiogenesis; diminishing ROS with potent antioxidants during placentation decreases placental angiogenesis and increases PE risk. Therefore, antioxidant therapy should be considered carefully for normal pregnant women during early gestation.
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Pepe, Gerald J., and Eugene D. Albrecht. "Novel Technologies for Target Delivery of Therapeutics to the Placenta during Pregnancy: A Review." Genes 12, no. 8 (August 17, 2021): 1255. http://dx.doi.org/10.3390/genes12081255.
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Uterine spiral artery remodeling is essential for placental perfusion and fetal growth and, when impaired, results in placental ischemia and pregnancy complications, e.g., fetal growth restriction, preeclampsia, premature birth. Despite the high incidence of adverse pregnancies, current treatment options are limited. Accordingly, research has shifted to the development of gene therapy technologies that provide targeted delivery of “payloads” to the placenta while limiting maternal and fetal exposure. This review describes the current strategies, including placental targeting peptide-bound liposomes, nanoparticle or adenovirus constructs decorated with specific peptide sequences and placental gene promoters delivered via maternal IV injection, directly into the placenta or the uterine artery, as well as noninvasive site-selective targeting of regulating genes conjugated with microbubbles via contrast-enhanced ultrasound. The review also provides a perspective on the effectiveness of these technologies in various animal models and their practicability and potential use for targeted placental delivery of therapeutics and genes in adverse human pregnancies affected by placental dysfunction.
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King, RG, NM Gude, Iulio JL Di, and SP Brennecke. "Regulation of human placental fetal vessel tone: role of nitric oxide." Reproduction, Fertility and Development 7, no. 6 (1995): 1407. http://dx.doi.org/10.1071/rd9951407.
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Factors affecting fetal vessel resistance have been studied in vitro in bilaterally perfused lobules of human placentae. Potent and efficacious constrictors in this preparation (in order of potency) include endothelin-1 > the thromboxane mimetic U46619 > endothelin-3 > prostaglandin F2 alpha. Inhibitors of eicosanoid synthesis did not affect fetal vessel basal perfusion pressure, nor did they potentiate the effects of the vasoconstrictor U46619. In contrast, the nitric oxide inhibitors N omega-nitro-L-arginine (NOLA), haemoglobin and methylene blue all increased fetal vessel basal perfusion pressure and also increased U46619-induced constriction. Similarly, NOLA markedly potentiated the constrictor effects of endothelin-1, angiotensin II, 5-hydroxytryptamine and bradykinin. These studies therefore provide evidence that NO is important in the maintenance of low basal fetal vessel impedance and also reduces the effects of a number of vasoconstrictor autacoids. Nitric oxide synthase (NOS) activity of human placental homogenates has been measured and shown to be mainly calcium-dependent. Human placental NOS activity was not affected by labour state but was reduced in pre-eclampsia. No evidence was found that in pre-eclampsia raised concentrations of the endogenous NOS inhibitor asymmetric dimethylarginine were responsible for the reduced placental NOS activity. Hence, these studies provide evidence that NO is an important endogenous dilator of the fetal vessels of the human placenta and that reduced NOS activity could contribute to the pathogenesis and/or effects of pre-eclampsia.
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GUDE, N. M., J. L. STEVENSON, E. K. MOSES, and R. G. KING. "Magnesium regulates hypoxia-stimulated apoptosis in the human placenta." Clinical Science 98, no. 4 (February 24, 2000): 375–80. http://dx.doi.org/10.1042/cs0980375.
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Apoptosis (programmed cell death) in the human placenta is likely to play a major role in determining the structure and function of that organ. Fetal growth restriction (FGR) has been shown to be associated with increased levels of placental apoptosis. Altered regulation of apoptosis may play an important pathophysiological role in FGR. As reduced placental perfusion and reduced oxygenation are features of FGR, one aim of this study was to determine the effects of hypoxia on apoptotic activity, as assessed by DNA laddering, of placental tissue in vitro. In addition, levels of placental apoptosis may be affected by pharmacological agents routinely used in obstetric patient management. Thus an additional aim of this study was to determine the effects of several relevant pharmacological agents on the levels of DNA laddering during in vitro incubation of human placentae under hypoxic conditions. Incubation of normal placental explant tissue at 37 °C for 1–2 h under hypoxic conditions significantly increased placental DNA laddering compared with that in non-incubated tissue, whereas levels of DNA laddering during incubation for up to 2 h under normoxic conditions were not significantly higher than those in non-incubated tissue. The DNA laddering activity of placental explants after 2 h of incubation under hypoxic conditions was significantly increased with increased concentrations of magnesium, but remained unchanged by the inclusion of pethidine, aspirin, nifedipine, dexamethasone, heparin or indomethacin in the incubation mixture. These results suggest that hypoxia may stimulate apoptotic activity in cultured human placental tissues, and that hypoxia-stimulated placental apoptosis may be further increased by increasing the extracellular magnesium concentration.
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Berveiller, Paul, Sophie Gil, and François Vialard. "Placental perfusion: interest and limits." Journal of Maternal-Fetal & Neonatal Medicine 30, no. 11 (August 8, 2016): 1347–48. http://dx.doi.org/10.1080/14767058.2016.1213807.
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Lewis, Rohan M., Jane K. Cleal, and Bram G. Sengers. "Placental perfusion and mathematical modelling." Placenta 93 (April 2020): 43–48. http://dx.doi.org/10.1016/j.placenta.2020.02.015.
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Kingdom, John C. P., and Sascha Drewlo. "Is heparin a placental anticoagulant in high-risk pregnancies?" Blood 118, no. 18 (November 3, 2011): 4780–88. http://dx.doi.org/10.1182/blood-2011-07-319749.
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Abstract Randomized control trials show beneficial effects of heparin in high-risk pregnancies to prevent preeclampsia and intrauterine growth restriction. However, the lack of placental pathology data in these trials challenges the assumption that heparin is a placental anticoagulant. Recent data show that placental infarction is probably associated with abnormalities in development of the placenta, characterized by poor maternal perfusion and an abnormal villous trophoblast compartment in contact with maternal blood, than with maternal thrombophilia. At-risk pregnancies may therefore be predicted by noninvasive prenatal testing of placental function in mid-pregnancy. Heparin has diverse cellular functions that include direct actions on the trophoblast. Dissecting the non–anticoagulant actions of heparin may indicate novel and safer therapeutic targets to prevent the major placental complications of pregnancy.
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Bapat, Priya, Reuven Kedar, Nir Melamed, Jeremy Matlow, Angelika Lubetsky, Katarina Aleksa, Howard Berger, and Gideon Koren. "The Transfer Of Dabigatran and Rivaroxaban Across a Dually Perfused Isolated Human Placental Cotyledon – Implications For Therapy In Pregnancy." Blood 122, no. 21 (November 15, 2013): 1142. http://dx.doi.org/10.1182/blood.v122.21.1142.1142.
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Abstract Background Anticoagulant therapy is often required in cases of high-risk pregnancy for the prophylaxis of venous thromboembolism following surgery, atrial fibrillation, and congestive heart failure, and for the prevention of pregnancy loss in thrombophilic women. During pregnancy, the concentrations of many blood-clotting factors rise, thereby increasing the need for anticoagulants that are safe to use throughout gestation. Dabigatran (Pradaxa®) and rivaroxaban (Xarelto®) are newer generation oral anticoagulants that are increasingly being prescribed to women of reproductive age for the treatment of thromboembolic disorders. Dabigatran acts by directly inhibiting thrombin, and rivaroxaban acts as a direct factor Xa inhibitor. However, the information regarding fetal safety and placental transfer of these drugs is currently lacking. If there is limited transfer of either drug across the placenta, then it may not increase the risk of bleeding in the fetus. The objective of this study was to determine the transplacental kinetics of dabigatran and rivaroxaban. Methods Placentae were obtained with informed consent after elective caesarean section of healthy term pregnancies in Toronto, Ontario. The transplacental transfer of dabigatran and rivaroxaban were separately assessed using ex vivo dual perfusion of an isolated human placental cotyledon. Dabigatran, at a concentration of 35 ng/ml, was added to the maternal circulation at the start of the experimental phase. Maternal and fetal samples were taken throughout the pre-experimental (1 h) and experimental (3 h) phases for measurement of dabigatran and markers of placental viability. Separate placenta perfusions with rivaroxaban were conducted at an initial maternal concentration of 250 ng/ml. The perfused drug was measured in maternal and fetal samples using liquid chromatography-mass spectrometry (LC/MS). Results There was slow transfer of dabigatran from the maternal to fetal circulation. The fetal-to-maternal (F:M) concentration ratio was 0.33 ± 0.13 after 3 hours (n=3). In contrast, the transfer of rivaroxaban from maternal to fetal circulation was much more rapid, as characterized by a F:M ratio of 0.72 ± 0.12 at 3 hour (n=4), suggesting rapid equilibrium between maternal and fetal circulations. Placental viability markers for all perfusions were within normal ranges. Conclusions This is the first direct evidence of the transfer of dabigatran and rivaroxaban across the human placenta from the mother to fetus. It suggests less fetal exposure to dabigatran. Disclosures: No relevant conflicts of interest to declare.
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Armstrong-Kempter, Shannon, Supuni Kapurubandara, Brian Trudinger, Noel Young, and Naim Arrage. "A Case of Placenta Percreta Managed with Sequential Embolisation Procedures." Case Reports in Obstetrics and Gynecology 2018 (2018): 1–7. http://dx.doi.org/10.1155/2018/7213689.
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Background. The incidence of morbidly adherent placenta, including placenta percreta, has increased significantly over recent years due to rising caesarean section rates. Historically, abnormally invasive placenta has been managed with caesarean hysterectomy; however nonsurgical interventions such as uterine artery embolisation (UAE) are emerging as safe alternative management techniques. UAE can be utilised to decrease placental perfusion and encourage placental resorption, thereby reducing the risk of haemorrhage and other morbidities. Case. We describe one of the very few reported cases of placenta percreta which was successfully treated primarily with sequential artery embolisation. Our patient underwent four embolisation procedures over a period of 248 days, with no major morbidity or complications. Conclusion. Repeat UAE may be a beneficial primary management modality in cases of placenta percreta with bladder involvement.
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Mathiesen, Line, Thit Aarøe Mørck, Marie Sønnegaard Poulsen, Jeanette Kolstrup Søgaard Nielsen, Tina Mose, Manhai Long, Eva Bonefeld‐Jørgensen, Rossana Bossi, and Lisbeth E. Knudsen. "Placental transfer of pesticides studied in human placental perfusion." Basic & Clinical Pharmacology & Toxicology 127, no. 6 (July 6, 2020): 505–15. http://dx.doi.org/10.1111/bcpt.13456.
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King, RG, NM Gude, BR Krishna, S. Chen, SP Brennecke, AL Boura, and TJ Rook. "Human placental acetylcholine." Reproduction, Fertility and Development 3, no. 4 (1991): 405. http://dx.doi.org/10.1071/rd9910405.
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The human placenta contains both acetylcholine (ACh) and choline acetyltransferase, and in vitro bilaterally perfused placental lobules release ACh. The function of this placental cholinergic system has not yet been clearly defined, although changes occur in it during parturition and it may be linked to placental prostaglandin generation at this time. It has also been suggested that ACh may regulate placental amino-acid transport and/or blood flow. It has been found that ACh release from fetal vessels of bilaterally perfused placental lobules is reduced during preeclampsia but is not necessarily correlated with any change in perfusion pressure or materno-fetal transfer of the nonmetabolizable amino acid alpha-aminoisobutyric acid. However, a correlation has been found between releases from human placental explants of ACh (when inhibited by (2-benzoylethyl)trimethylammonium or vesamicol) and of prostaglandins E2 and F2 alpha. Thus, although the evidence for a role of ACh in the control of placental amino-acid transfer or vascular tone is not conclusive, inhibition of the human placental cholinergic system has been shown to be associated with reduced output of prostaglandins from this tissue.
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Zhang, Meng-Ling, Qian Yang, Yan-Di Zhu, Ya-Di Zhang, Rui Zhang, Jian Liu, Xiao-Yan Zhao, et al. "Nobiletin Inhibits Hypoxia-Induced Placental Damage via Modulating P53 Signaling Pathway." Nutrients 14, no. 11 (June 1, 2022): 2332. http://dx.doi.org/10.3390/nu14112332.
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In this study, we aimed to evaluate the effect of Nobiletin (NOB) on the placenta of Sprague–Dawley (SD) rats that had undergone reduced uterine perfusion pressure (RUPP) surgery and to evaluate the safety of NOB intervention during pregnancy. The results showed that NOB alleviated placental hypoxia, attenuated placental cell apoptosis, and inhibited placental damage in RUPP rats. No side effect of NOB intervention during pregnancy was observed. BeWo cell lines with P53 knockdown were then constructed using lentiviral transfection, and the P53 signaling pathway was found to be essential for NOB to reduce hypoxia-induced apoptosis of the BeWo cell lines. In summary, NOB attenuated hypoxia-induced placental damage by regulating the P53 signaling pathway, and those findings may contribute some insights into the role of NOB in placental development and the prevention of placental-related diseases.
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T., Ramya, Umamaheswari G., and Chaitra V. "Placental pathology in maternal autoimmune diseases-new insights and clinical implications." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 6, no. 9 (August 28, 2017): 4090. http://dx.doi.org/10.18203/2320-1770.ijrcog20174067.
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Background: Pregnancy in women with autoimmune diseases is frequently associated with placental insufficiency leading to adverse perinatal outcome. Aim of the study was to investigate the presence and possible clinical significance of placental lesions in mothers with different autoimmune disorders.Methods: In this retrospective study, 11 placentas from 10 mothers with diverse autoimmune diseases including systemic lupus Erythematosus (SLE), antiphospholipid antibodies (APLA), idiopathic thrombocytopenic purpura (ITP) and antinuclear antibodies (ANA) were studied.Results: Placental correlates were reduced placental weight, maternal vascular under perfusion, abruption, villitis of unknown etiology, multifocal chorangiomatosis, distal villous immaturity, massive perivillous fibrin deposition/maternal floor infarction and foetal thrombotic vasculopathy. Of the 11 pregnancies 3 were untreated (1 SLE, 2 APLA) and resulted in intrauterine foetal demise. The lesions were more severe in these cases. All the treated pregnancies resulted in live born babies (8), of which 3 were growth restricted, 2 were complicated with oligohydramnios and 3 were delivered preterm.Conclusions: In this group of diverse autoimmune disorders, placental lesions were not specific for each of them. Apart from maternal vascular under perfusion, lesions like villitis of unknown etiology, distal villous immaturity and massive perivillous fibrin deposition were identified and may recur in subsequent pregnancies and treatment should be directed towards modifying it. The placental examination should be mandatory in all cases of maternal autoimmunity and pregnancies with poor foetal outcome.
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Deloison, Benjamin, Chloé Arthuis, Gabriel Benchimol, Daniel Balvay, Laurence Bussieres, Anne-Elodie Millischer, David Grévent, et al. "Human placental perfusion measured using dynamic contrast enhancement MRI." PLOS ONE 16, no. 9 (September 2, 2021): e0256769. http://dx.doi.org/10.1371/journal.pone.0256769.
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Objectives To evaluate the feasibility of dynamic contrast enhanced magnetic resonance imaging (DCE MRI) and measure values of in vivo placental perfusion in women. Methods This study was part of the Placentimage trial (NCT01092949). Gadolinium-chelate (Gd) enhanced dynamic MRI was performed two days before termination of pregnancies at 16 to 34 weeks gestational age (GA). Quantitative analysis was performed using one-compartment intravascular modeling. DCE perfusion parameters were analyzed across GA and were compared in IUGR and AGA fetuses. Results 134 patients were enrolled. After quality control check, 62 DCE MRI were analyzed including 48 and 14 pregnancies with normal and abnormal karyotypes, respectively. Mean placental blood flow was 129±61 mL/min/100ml in cases with normal karyotypes. Fetuses affected by IUGR (n = 13) showed significantly lower total placental blood flow values than AGA fetuses (n = 35) (F total = 122±88 mL/min versus 259±34 mL/min, p = 0.002). DCE perfusion parameters showed a linear correlation with GA. Conclusions Measuring placental perfusion in vivo is possible using DCE MRI. Although this study has many limitations it gives us the first DCE MRI values that provide a potential standard for future research into placental perfusion methods and suggests that placental functional parameters are altered in IUGR pregnancies.
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Delforce, Sarah J., Eugenie R. Lumbers, Stacey J. Ellery, Padma Murthi, and Kirsty G. Pringle. "Dysregulation of the placental renin–angiotensin system in human fetal growth restriction." Reproduction 158, no. 3 (September 2019): 237–45. http://dx.doi.org/10.1530/rep-18-0633.
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Fetal growth restriction (FGR) is a pregnancy complication wherein the foetus fails to reach its growth potential. The renin–angiotensin system (RAS) is a critical regulator of placental function, controlling trophoblast proliferation, angiogenesis and blood flow. The RAS significantly influences uteroplacental blood flow through the balance of its vasoconstrictive and vasodilatory pathways. Although the RAS is known to be dysregulated in placentae from women with preeclampsia, the expression of the RAS has not yet been studied in pregnancies compromised by FGR alone. This study investigated the mRNA expression and protein levels of RAS components in placentae from pregnancies compromised by FGR. Angiotensin II type 1 receptor (AGTR1) and angiotensin-converting enzyme 2 (ACE2) mRNA levels were reduced in FGR placentae compared with control (P = 0.012 and 0.018 respectively). Neprilysin (NEP) mRNA expression was lower in FGR placentae compared with control (P = 0.004). mRNA levels of angiotensinogen (AGT) tended to be higher in FGR placentae compared with control (P = 0.090). Expression of prorenin, AGT, angiotensin-converting enzyme (ACE) or ACE2 proteins were similar in control and FGR placentae. The renin-AGT reaction is a first order reaction so levels of expression of placental AGT determine levels of Ang II. Decreasing levels of ACE2 and/or NEP by limiting the production of Ang-(1-7), which is a vasodilator, and increasing placental Ang II levels (vasoconstrictor) may result in an imbalance between the vasoconstrictor and vasodilator arms of the placental RAS. Ultimately this dysregulation of the placental RAS could lead to reduced placental perfusion that is evident in FGR.
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Shaw, A. J., M. Z. Mughal, M. J. A. Maresh, and C. P. Sibley. "Effects of two synthetic parathyroid hormone-related protein fragments on maternofetal transfer of calcium and magnesium and release of cyclic AMP by the in-situ perfused rat placenta." Journal of Endocrinology 129, no. 3 (June 1991): 399–404. http://dx.doi.org/10.1677/joe.0.1290399.
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ABSTRACT Two human parathyroid hormone-related protein (hPTHrP) fragments were tested for effects on maternofetal transfer of 45Ca and Mg across the in-situ perfused rat placenta at 21 days of gestation (term = 23 days). The fetal placental circulation was perfused with a Mg-free Krebs–Ringer solution and the unidirectional maternofetal clearance (Kmf) of 45Ca and Mg compared with that of 51Cr-EDTA, the latter being employed as a paracellular diffusional marker. Placental perfusion with hPTHrP(1–34) (100 ng/ml) or hPTHrP(75–86)amide (50 ng/ml) did not significantly alter the Kmf of 45Ca or that of Mg. In separate rats, however, hPTHrP(1–34) but not hPTHrP(75–86)amide stimulated marked placental cyclic AMP (cAMP) release, the peak response of 63±7 pmol/min occurring 10 min after the beginning of the peptide perfusion. A lower dose of hPTHrP(1–34) (4 ng/ml) produced a similar peak release of cAMP, as did [Nle8,21,Tyr34]-rPTH(1–34)amide (4 ng/ml) and the adenylate cyclase agonist forskolin (17 μmol/l). Forskolin also rapidly increased the Kmf of 45Ca but not that of Mg or 51Cr-EDTA. The present study indicates that hPTHrP does not acutely affect maternofetal transfer of Ca or Mg across the perfused rat placenta. The data also question the role played by cAMP in the stimulatory actions of forskolin on placental Ca transport. Journal of Endocrinology (1991) 129, 399–404
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Sankaralingam, Sowndramalingam, Ivan A. Arenas, Manoj M. Lalu, and Sandra T. Davidge. "Preeclampsia: current understanding of the molecular basis of vascular dysfunction." Expert Reviews in Molecular Medicine 8, no. 3 (January 26, 2006): 1–20. http://dx.doi.org/10.1017/s1462399406010465.
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Preeclampsia is a pregnancy-specific disorder characterised by hypertension and proteinuria occurring after the 20th week of gestation. Delivery of the placenta results in resolution of the condition, implicating the placenta as a central culprit in the pathogenesis of preeclampsia. In preeclampsia, an inadequate placental trophoblast invasion of the maternal uterine spiral arteries results in poor placental perfusion, leading to placental ischaemia. This could result in release of factors into the maternal circulation that cause widespread activation or dysfunction of the maternal endothelium. Factors in the maternal circulation might induce oxidative stress and/or elicit an inflammatory response in the maternal endothelium, resulting in the altered expression of several genes involved in the regulation of vascular tone. This review addresses the potential circulating factors and the molecular mechanisms involved in the alteration of vascular function that occurs in preeclampsia.
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Broekhuizen, Michelle, Theo Klein, Emilie Hitzerd, Yolanda B. de Rijke, Sam Schoenmakers, Peter Sedlmayr, A. H. Jan Danser, Daphne Merkus, and Irwin K. M. Reiss. "l -Tryptophan–Induced Vasodilation Is Enhanced in Preeclampsia." Hypertension 76, no. 1 (July 2020): 184–94. http://dx.doi.org/10.1161/hypertensionaha.120.14970.
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l -tryptophan induces IDO (indoleamine 2,3-dioxygenase) 1–dependent vasodilation. IDO1 is expressed in placental endothelial cells and downregulated in preeclampsia. Hypothesizing that this may contribute to diminished placental perfusion, we studied l -tryptophan–induced vasodilation in healthy and early-onset preeclampsia placental arteries, focusing on placental kynurenine pathway alterations. Despite IDO1 downregulation, kynurenine pathway metabolite concentrations (measured with ultra-performance liquid chromatography-tandem mass spectrometry) were unaltered in preeclamptic versus healthy placentas. Most likely, this is due to enhanced l -tryptophan uptake, evidenced by increased l -tryptophan levels in preeclamptic placentas. Ex vivo perfused cotyledons from healthy and preeclamptic placentas released similar amounts of l -tryptophan and kynurenine pathway metabolites into the circulations. This release was not altered by adding l -tryptophan in the maternal circulation, suggesting that l -tryptophan metabolites act intracellularly. Maternally applied l -tryptophan did appear in the fetal circulation, confirming placental passage of this essential amino acid. After in vitro incubation of placental arteries with IDO1-upregulating cytokines interferon-γ and tumor necrosis factor-α, l -tryptophan induced vasodilation. This vasodilation was attenuated by both IDO1 and nitric oxide (NO) synthase inhibitors. Despite IDO1 downregulation, l -tryptophan–induced relaxation was enhanced in preeclamptic versus healthy placental arteries. However, cytokine stimulation additionally upregulated the LAT ( l -type amino acid transporter) 1 in preeclamptic placental arteries only. Vasodilation to the lipophilic, transporter independent ethyl ester of l -tryptophan was reduced in preeclamptic versus healthy placental arteries, in agreement with reduced IDO1 expression. In conclusion, l -tryptophan induces IDO1- and NO-dependent relaxation in placental arteries, which is determined by l -tryptophan uptake rather than IDO1 expression. Increased l -tryptophan uptake might compensate for reduced IDO1 expression in preeclamptic placentas.
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Ceesay, M. Mansour, Sameer Tulpule, Sergio Querol, Linda Barber, Terie Duffy, Bronwen E. Shaw, J. Alejandro Madrigal, Ghulam J. Mufti, and Antonio Pagliuca. "Plerixafor Ex Vivo Mobilization of Placental Derived Haematopoietic Stem Cells." Blood 118, no. 21 (November 18, 2011): 4790. http://dx.doi.org/10.1182/blood.v118.21.4790.4790.
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Abstract Abstract 4790 Introduction The utility of cord blood as an alternative source of stem cells for haematopoietic stem cell transplantation is well established in the paediatric population. Although it's use in adults has surged over the past few years there are still problems associated with a low stem cell dose which may lead to delayed engraftment, incomplete and inefficient immune reconstitution, and poor survival. Various techniques have been used to increase the stem cell dose including ex vivo expansion, the use of double cords, intrabone injections and the use of third party donor cells. Using standard collection techniques only about 25% of cord blood samples collected reach the target cell dose in adults. The placenta is a rich source of CD34+ cells which may not be fully mobilised using current cord blood collection techniques. A modified two-step collection technique in which the initial collection is followed by placental perfusion with 50 ml heparinised 0.9% saline has shown a 15% increase in the number of nucleated cells. We have modified this technique further by perfusing the placenta with Plerixafor, a CXCR4 antagonist that is currently licensed in the UK for mobilisation of autologous stem cells from adults. The study aim was to assess whether plerixafor could enhance recovery of CD34+ cells and change the immune profile of the perfusate. Method Ten cord blood units were collected as per our standard operating procedures. After cord blood collection, 5 placentas were perfused with 50 ml 0.9% saline plus 5,000 units of preservative free heparin by slow infusion over 50 minutes and perfusate collected after about 5 minutes of starting the infusion over 50 minutes (controls). The other 5 placentas were treated the same way except for the addition of 24 mg Plerixafor to the 50 ml 0.9% saline plus 5,000 units of preservative free heparin and collected as per control arm (plerixafor arm). The samples were analysed by multicolour flow cytometry using a combination of antibody cocktails to identify and enumerate CD34+ stem cells, T cells, T cell precursors, T cell subsets, T regulatory cells, B cells, NK and NK cell precursors, and Dendtritic cells. The CD34+ progenitor cells were further quantified by CFU – a methylcellulose media based assay. Results Successful recovery of perfusate was achieved from 9 placentas (mean volume 44 ml +/− SEM 4.7) as one of the collected samples clotted. There was no significant difference in the perfusate volumes between the 2 arms (48ml v 38ml, P=0.152). Percentage increase in numbers of cells recovered by perfusing the placenta was calculated from total numbers of CD34+ and CD45+ cells collected from each cord and placenta pair. Plerixafor did not significantly increase the recovery of cells from the placenta. Perfusion of the 5 control placentas increased recovery of CD34+ cell by 5.06% (mean +/− 0.89 SEM) and CD45+ cells by 4.69% (mean +/−1.09 SEM). Perfusion of 4 placentas with saline plus Plerixafor increased recovery of CD34+ cells by 5.79% (mean +/−2.17 SEM) and CD45+ cells by 2.61% (mean +/− 0.79 SEM). Viability of haematopoietic stem cell progenitors was assessed by colony formation assay with no significant difference detected between the control arm (mean 18.4 CFU +/− 8.26 SEM; n=5) and the plerixafor arm (mean 4.8 CFU +/− 2.7 SEM; n=4). There was no significant difference in the number of CD34+ cells recovered from the controls as compared to their corresponding cords (n=5, paired t test, p= 0.054). Similarly, there was no significant difference in the plerixafor arm (n=4, paired t test, p=0.091). There was no significant increase in the number of CD34+ stem cells recovered from the plerixafor group as compared to the control group (unpaired t test, p=0.74). There was no significant increase in the number of CD45+ cells in the plerixafor arm compared to the controls (unpaired t test, p= 0.4). Similarly there was no significant difference in the clonal efficiency of the between the 2 groups (unpaired t test, p=0.2). There were no significant differences in the CD3, CD4, CD8 T cells, Tregs, NK, DCs, progenitor T and NK cells between the 2 groups. Conclusion In this pilot study plerixafor does not seem to significantly increase the CD34+ stem cells and other cell subsets. It is possible that the duration of infusion was too short to mobilise the stem cells. Further studies are warranted to investigate this further. Disclosures: Off Label Use: Plerixafor for stem cell mobilzation from placenta. Shaw:Therakos, a Johnson and Johnson company: Honoraria, Speakers Bureau.
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Kupper, Nadja, Elisabeth Pritz, Monika Siwetz, Jacqueline Guettler, and Berthold Huppertz. "Placental Villous Explant Culture 2.0: Flow Culture Allows Studies Closer to the In Vivo Situation." International Journal of Molecular Sciences 22, no. 14 (July 12, 2021): 7464. http://dx.doi.org/10.3390/ijms22147464.
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During pregnancy, freely floating placental villi are adapted to fluid shear stress due to placental perfusion with maternal plasma and blood. In vitro culture of placental villous explants is widely performed under static conditions, hoping the conditions may represent the in utero environment. However, static placental villous explant culture dramatically differs from the in vivo situation. Thus, we established a flow culture system for placental villous explants and compared commonly used static cultured tissue to flow cultured tissue using transmission and scanning electron microscopy, immunohistochemistry, and lactate dehydrogenase (LDH) and human chorionic gonadotropin (hCG) measurements. The data revealed a better structural and biochemical integrity of flow cultured tissue compared to static cultured tissue. Thus, this new flow system can be used to simulate the blood flow from the mother to the placenta and back in the most native-like in vitro system so far and thus can enable novel study designs.
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Bowkalow, Sandy, Ekkehard Schleussner, Christiane Kähler, Uwe Schneider, Thomas Lehmann, and Tanja Groten. "Pentaerythrityltetranitrate (PETN) improves utero- and feto-placental Doppler parameters in pregnancies with impaired utero-placental perfusion in mid-gestation – a secondary analysis of the PETN-pilot trial." Journal of Perinatal Medicine 46, no. 9 (November 27, 2018): 1004–9. http://dx.doi.org/10.1515/jpm-2017-0238.
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AbstractAim:In pregnancies complicated by impaired utero-placental perfusion, pentaeritrithyltetranitrate (PETN) has been shown to reduce the risk of severe fetal growth restriction (FGR) and perinatal death by 39%. The effect is most likely related to the vasodilatative influence of PETN. To assess its impact on utero-placental and fetal perfusion, we analyzed the Doppler parameters measured during the PETN pilot-trial.Methods:One hundred and eleven pregnancies presenting impaired utero-placental resistance at mid-gestation were included in the trial. Fifty-four women received PETN, while 57 received a placebo. Doppler velocimetry measurements were monitored biweekly. Statistical analysis was performed using a mixed linear model.Results:Within the first week of treatment, the mean pulsatility index (PI) of the uterine artery (UtA) dropped more prominently in the PETN group [−0.20, 95% confidence interval (CI): −0.34 to −0.05, P=0.007). The adjusted relative risk (RR) for abnormal cerebro-placental ratio (CPR) was significantly reduced by PETN [RR 0.412 (95% CI: 0.181–0.941)]. Kaplan-Meier analysis demonstrates the postponement of absent end-diastolic flow (AED), absent or reverse end-diastolic flow (ARED), brain sparing and abnormal cerebroplacental ratio (CPR) in the PETN group.Conclusion:The demonstrated effect of PETN on utero-placental and feto-placental perfusion strengthens the evidence for a positive impact in pregnancies complicated by impaired placental perfusion and might explain the effect on neonatal outcome, as shown in the PETN-pilot trial.
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Francis, Susan T., Keith R. Duncan, Rachel J. Moore, Philip N. Baker, Ian R. Johnson, and Penny A. Gowland. "Non-invasive mapping of placental perfusion." Lancet 351, no. 9113 (May 1998): 1397–99. http://dx.doi.org/10.1016/s0140-6736(97)07089-x.
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Sitepu, M., A. Syahriza, D. Sibuea, and T. M. Hanafiah. "Placental perfusion in 3rd trimester pregnancy." IOP Conference Series: Earth and Environmental Science 125 (March 2018): 012191. http://dx.doi.org/10.1088/1755-1315/125/1/012191.
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Jauniaux, Eric, J. Gonzalo Moscoso, Michel Vanesse, Stuart Campbell, and Marie Driver. "Perfusion fixation for placental morphologic investigation." Human Pathology 22, no. 5 (May 1991): 442–49. http://dx.doi.org/10.1016/0046-8177(91)90129-d.
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Hirschmugl, Birgit, Waltraud Brandl, Bence Csapo, Mireille van Poppel, Harald Köfeler, Gernot Desoye, Christian Wadsack, and Evelyn Jantscher-Krenn. "Evidence of Human Milk Oligosaccharides in Cord Blood and Maternal-to-Fetal Transport across the Placenta." Nutrients 11, no. 11 (November 4, 2019): 2640. http://dx.doi.org/10.3390/nu11112640.
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Human milk oligosaccharides (HMOs) are present in maternal serum in early gestation, raising the question of whether HMOs can cross the placental barrier and reach fetal circulation. Here, we aimed to detect HMOs in cord blood, and assess HMO composition and concentration in relation to maternal HMOs. In an ex-vivo placental perfusion model, we asked whether HMOs can pass over the placenta. Using HPLC, we measured HMOs in maternal serum and matching venous cord blood samples collected at delivery from normal pregnancies (n = 22). To investigate maternal-to-fetal transport, we perfused isolated placental cotyledons from term pregnancies (n = 3) with 2’-fucosyllactose (2′FL) in a double closed setting. We found up to 18 oligosaccharides typically present in maternal serum in all cord serum samples investigated. Median total cord blood HMO concentration did not differ from the concentration in maternal serum. HMO composition resembled the composition in maternal serum, with the strongest correlations for 2′FL and LDFT. After 180 min perfusion, we found 22% of maternally offered 2′FL in the fetal circuit without reaching equilibrium. Our results provide direct evidence of HMOs in cord blood, and suggest that the placenta transfers HMOs from the maternal to fetal circuit. Future studies will investigate potential differences in the transfer of specific HMOs, or in pregnancy disorders.
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Hirschmugl, Birgit, Simone Perazzolo, Bram G. Sengers, Rohan M. Lewis, Michael Gruber, Gernot Desoye, and Christian Wadsack. "Placental mobilization of free fatty acids contributes to altered materno-fetal transfer in obesity." International Journal of Obesity 45, no. 5 (February 26, 2021): 1114–23. http://dx.doi.org/10.1038/s41366-021-00781-x.
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Abstract Background Metabolic changes in obese pregnant women, such as changes of plasma lipids beyond physiological levels, may subsequently affect fetal development in utero. These metabolic derangements may remain in the offspring and continue throughout life. The placenta mediates bidirectional exchange of nutrients between mother and fetus. The impact of prepregnancy obesity on placental transfer of lipids is still unknown. Objective We aimed to examine materno-to-fetal free fatty acid (FFA) transfer by a combined experimental and modeling approach. Flux of 13C-labeled FFA was evaluated by ex vivo perfusion of human placentae as a function of prepregnancy obesity. Mathematical modeling complemented ex vivo results by providing FFA kinetic parameters. Results Obesity was strongly associated with elevated materno-to-fetal transfer of applied 13C-FFA. Clearance of polyunsaturated 13C-docosahexaenoic acid (DHA) was most prominently affected. The use of the mathematical model revealed a lower tissue storage capacity for DHA in obese compared with lean placentae. Conclusion Besides direct materno-to-fetal FFA transfer, placental mobilization accounts for the fetal FA supply. Together, with metabolic changes in the mother and an elevated materno-fetal FFA transfer shown in obesity, these changes suggest that they may be transmitted to the fetus, with yet unknown consequences.
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Rada, Cara C., Grace Murray, and Sarah K. England. "The SK3 channel promotes placental vascularization by enhancing secretion of angiogenic factors." American Journal of Physiology-Endocrinology and Metabolism 307, no. 10 (November 15, 2014): E935—E943. http://dx.doi.org/10.1152/ajpendo.00319.2014.
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Proper placental perfusion is essential for fetal exchange of oxygen, nutrients, and waste with the maternal circulation. Impairment of uteroplacental vascular function can lead to pregnancy complications, including preeclampsia and intrauterine growth restriction (IUGR). Potassium channels have been recognized as regulators of vascular proliferation, angiogenesis, and secretion of vasoactive factors, and their dysfunction may underlie pregnancy-related vascular diseases. Overexpression of one channel in particular, the small-conductance calcium-activated potassium channel 3 (SK3), is known to increase vascularization in mice, and mice overexpressing the SK3 channel (SK3T/T mice) have a high rate of fetal demise and IUGR. Here, we show that overexpression of SK3 causes fetal loss through abnormal placental vascularization. We previously reported that, at pregnancy day 14, placentas isolated from SK3T/T mice are smaller than those obtained from wild-type mice. In this study, histological analysis reveals that SK3T/− placentas at this stage have abnormal placental morphology, and microcomputed tomography shows that these placentas have significantly larger and more blood vessels than those from wild-type mice. To identify the mechanism by which these vascularization defects occur, we measured levels of vascular endothelial growth factor (VEGF), placental growth factor, and the soluble form of VEGF receptor 1 (sFlt-1), which must be tightly regulated to ensure proper placental development. Our data reveal that overexpression of SK3 alters systemic and placental ratios of the angiogenic factor VEGF to antiangiogenic factor sFlt-1 throughout pregnancy. Additionally, we observe increased expression of hypoxia-inducing factor 2α in SK3T/− placentas. We conclude that the SK3 channel modulates placental vascular development and fetal health by altering VEGF signaling.