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Artykuły w czasopismach na temat "Placental perfusion"
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Mose, Tina, Lisbeth E. Knudsen, Morten Hedegaard i Gerda K. Mortensen. "Transplacental Transfer of Monomethyl Phthalate and Mono(2-ethylhexyl) Phthalate in a Human Placenta Perfusion System". International Journal of Toxicology 26, nr 3 (maj 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 i SP Brennecke. "Endothelin: release by and potent constrictor effect on the fetal vessels of human perfused placental lobules". Reproduction, Fertility and Development 3, nr 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 i 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, nr 5 (1.05.1995): 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 i C. P. Sibley. "Sodium-dependent magnesium transport across in situ perfused rat placenta". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, nr 2 (1.08.1991): 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., i Graeme N. Smith. "The effect of nicotine on in vitro placental perfusion pressure". Canadian Journal of Physiology and Pharmacology 84, nr 8-9 (wrzesień 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 i Carolyn L. Bayer. "Longitudinal characterization of local perfusion of the rat placenta using contrast-enhanced ultrasound imaging". Interface Focus 9, nr 5 (16.08.2019): 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, i Sarah Cajusay-Velasco. "Three-dimensional Power Doppler Ultrasound Study of the Placenta". Donald School Journal of Ultrasound in Obstetrics and Gynecology 8, nr 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 i F. L. Hanley. "Extracorporeal circulation in the isolated in situ lamb placenta: hemodynamic characteristics". Journal of Applied Physiology 72, nr 6 (1.06.1992): 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 i Ya Ping Shi. "Evaluation of Various Methods of Maternal Placental Blood Collection for Immunology Studies". Clinical and Vaccine Immunology 13, nr 5 (maj 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 i 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, nr 2 (maj 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
Rozprawy doktorskie na temat "Placental perfusion"
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Hutchinson, Elizabeth S. "Use of the placental perfusion model to investigate the placental origins of pre-eclampsia". Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499908.
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Vanderlelie, Jessica, i n/a. "Placental Oxidative Stress in Preeclampsia". Griffith University. School of Medical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20060918.161726.
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Affecting 6-8% of all pregnancies, preeclampsia is the leading cause of maternal morbidity in the western world and is charactensed by hypertension, proteinuria, edema and platelet aggregation. Despite its prevalence and severity, no comprehensive theory or single factor has been suggested to explain the pathophysiology of this multi system disorder of pregnancy, with the only therapies being bed rest, pharmacological symptom management and if necessary early delivery. Oxidative stress plays an important role in the pathophysiology of preeclampsia, resulting from defective trophoblast invasion, reductions in placental perfusion and placental hypoxia/reoxygenation. The inability of endogenous antioxidant systems up regulated in normal pregnancy, to control increased levels of oxidative stress, is suggested as a possible factor in the feed forward generation of reactive oxygen species and placental oxidative stress. That in turn may stimulate increased syncytiotrophoblast apoptosis, endothelial cell activation and the maternal hyper immune response characteristic of preeclampsia. Analysis of the research literature revealed that previous evaluations of placental oxidation and antioxidant enzyme activity in preeclampsia were by no means comprehensive, and exhibited significant inter-study variations. It was the aim of this thesis to clarify the placental oxidative state and the endogenous antioxidant activity of glutathione peroxidase, thioredoxin reductase, thioredoxin and superoxide dismutase in human placentae in an attempt to determine if variations in antioxidant function were due to changes in gene expression or protein oxidation. The findings reported in this thesis indicate the presence of increased levels of oxidative stress in the preeclamptic placenta, associated with significant reductions in antioxidant enzyme capacity. Quantitative real-time PCR analysis of placental samples revealed that deceases in antioxidant capacity in the placenta are more likely to be related to the significant oxidative burden within the tissue rather than reductions in gene expression. A number of animal models exist to investigate components of preeclampsia pathophysiology, however the ability of these models to mimic the oxidative and antioxidant features of preeclampsia remains unclear. The exposure of pregnant rats to N(G)-nitro-L-arginine methyl ester is a widely used model of endothelial cell dysfunction during preeclampsia. It was the aim of this thesis to determine the biochemical characteristics of this model in an attempt to assess its effectiveness in mimicking oxidative changes in the preeclamptic placenta. Although this model is capable of producing a syndiome in rats similar to the disorder in terms of physiology, this is not manifest in terms of placental biochemistry. The importance of selenium in the synthesis of selenobased antioxidants such as glutathione peroxidase and thioredoxin reductase is well documented. Increasing demand for selenium by the developing fetus may be linked to reductions in selenium status during pregnancy. Considering preeclampsia is associated with significant reductions in selenium status it may be hypothesised that reductions in antioxidant function may be linked to selenium inadequacy. The modulation of dietary selenium in pregnant rats was used to determine the importance of selenium during pregnancy and its effect on antioxidant function and placental oxidative stress. The results of this analysis revealed that selenium deficiency causes a pregnancy specific condition similar to preeclampsia. This condition was found to be associated with increased placental oxidative stress and significant reductions in the systemic activity of selenobased antioxidants that could be modified through selenium supplementation. In summary, data obtained in this thesis indicate that placental oxidative stress and reduced antioxidant enzyme activity play a significant role in the pathogenesis of preeclampsia. These studies support the hypothesis that antioxidant sufficiency is crucial in the maintenance of oxidative balance and that antioxidant dysfunction may result in damage to the placenta and the progression of the disease. These novel data further our understanding of the pathophysiology of preeclampsia and provide new insight into the pathogenesis of clinical complications exhibited in this condition, suggesting antioxidant therapy as a possible means for improving the health outcomes of both mother and baby.
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Vanderlelie, Jessica. "Placental Oxidative Stress in Preeclampsia". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365679.
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Affecting 6-8% of all pregnancies, preeclampsia is the leading cause of maternal morbidity in the western world and is charactensed by hypertension, proteinuria, edema and platelet aggregation. Despite its prevalence and severity, no comprehensive theory or single factor has been suggested to explain the pathophysiology of this multi system disorder of pregnancy, with the only therapies being bed rest, pharmacological symptom management and if necessary early delivery. Oxidative stress plays an important role in the pathophysiology of preeclampsia, resulting from defective trophoblast invasion, reductions in placental perfusion and placental hypoxia/reoxygenation. The inability of endogenous antioxidant systems up regulated in normal pregnancy, to control increased levels of oxidative stress, is suggested as a possible factor in the feed forward generation of reactive oxygen species and placental oxidative stress. That in turn may stimulate increased syncytiotrophoblast apoptosis, endothelial cell activation and the maternal hyper immune response characteristic of preeclampsia. Analysis of the research literature revealed that previous evaluations of placental oxidation and antioxidant enzyme activity in preeclampsia were by no means comprehensive, and exhibited significant inter-study variations. It was the aim of this thesis to clarify the placental oxidative state and the endogenous antioxidant activity of glutathione peroxidase, thioredoxin reductase, thioredoxin and superoxide dismutase in human placentae in an attempt to determine if variations in antioxidant function were due to changes in gene expression or protein oxidation. The findings reported in this thesis indicate the presence of increased levels of oxidative stress in the preeclamptic placenta, associated with significant reductions in antioxidant enzyme capacity. Quantitative real-time PCR analysis of placental samples revealed that deceases in antioxidant capacity in the placenta are more likely to be related to the significant oxidative burden within the tissue rather than reductions in gene expression. A number of animal models exist to investigate components of preeclampsia pathophysiology, however the ability of these models to mimic the oxidative and antioxidant features of preeclampsia remains unclear. The exposure of pregnant rats to N(G)-nitro-L-arginine methyl ester is a widely used model of endothelial cell dysfunction during preeclampsia. It was the aim of this thesis to determine the biochemical characteristics of this model in an attempt to assess its effectiveness in mimicking oxidative changes in the preeclamptic placenta. Although this model is capable of producing a syndiome in rats similar to the disorder in terms of physiology, this is not manifest in terms of placental biochemistry. The importance of selenium in the synthesis of selenobased antioxidants such as glutathione peroxidase and thioredoxin reductase is well documented. Increasing demand for selenium by the developing fetus may be linked to reductions in selenium status during pregnancy. Considering preeclampsia is associated with significant reductions in selenium status it may be hypothesised that reductions in antioxidant function may be linked to selenium inadequacy. The modulation of dietaty selenium in pregnant rats was used to determine the importance of selenium during pregnancy and its effect on antioxidant function and placental oxidative stress. The results of this analysis revealed that selenium deficiency causes a pregnancy specific condition similar to preeclampsia. This condition was found to be associated with increased placental oxidative stress and significant reductions in the systemic activity of selenobased antioxidants that could be modified through selenium supplementation. In summary, data obtained in this thesis indicate that placental oxidative stress and reduced antioxidant enzyme activity play a significant role in the pathogenesis of preeclampsia. These studies support the hypothesis that antioxidant sufficiency is crucial in the maintenance of oxidative balance and that antioxidant dysfunction may result in damage to the placenta and the progression of the disease. These novel data further our understanding of the pathophysiology of preeclampsia and provide new insight into the pathogenesis of clinical complications exhibited in this condition, suggesting antioxidant therapy as a possible means for improving the health outcomes of both mother and baby.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Full Text
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Myllynen, P. (Päivi). "In search of models for hepatic and placental pharmacokinetics". Doctoral thesis, University of Oulu, 2003. http://urn.fi/urn:isbn:9514270231.
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Abstract
Several in vitro methods using both human and animal tissues have been developed to study hepatic metabolism and placental transfer. The pressure to minimize animal studies has increased during the past few decades due to the public opinion and ethical considerations. However, these methods need further evaluation of their predictive power when applied in vivo. The aim of this work was to produce new information of the metabolism and transplacental passage of several anticonvulsants as well as to evaluate the usefulness of the placental perfusion method and several in vitro methods for analyzing metabolism in the prediction of clinical pharmacokinetics.
Carbamazepine (CBZ) metabolism was studied using human and mouse liver microsomes, human hepatocytes, human liver slices and yeast cells expressing recombinant enzymes. All test systems predicted well the major metabolite carbamazepine-10,11-epoxide (CBZ-E). Also, minor metabolites were produced in slightly variable amounts in all systems except cells with recombinant enzymes. All human liver systems demonstrated that CYP3A4 is the principal CBZ metabolising enzyme. However, our results on CBZ-treated mice suggested that the metabolism of CBZ to CBZ-E is mainly mediated by CYP1A1 in C57/BL6 mice. Autoinduction of CBZ metabolism was seen in hepatocytes and in incubations using microsomes from CBZ-treated mice. Human liver and mouse liver microsomes metabolized oxcarbazepine (OCBZ) mainly to its active metabolite, 10-hydroxy-10,11-dihydro-carbamazepine (10-OH-CBZ). Also, 10,11-trans-dihydroxy-10,11-dihydro-carbamazepine (10,11-D) and an unknown metabolite were detected.
Placental transfer of lamotrigine (LTG) and diazepam (DZP) was considerable in the human placental perfusion system, indicating marked fetal exposure in vivo. The OCBZ, 10-OH-CBZ and 10,11-D analyzed from maternal venous and cord blood also suggested significant fetal exposure. The placental perfusion system predicts well the transplacental passage of LTG and OCBZ and its major metabolite. However, in vivo cord blood concentrations of DZP are higher than maternal concentrations. Placental perfusion studies did not predict this. Still, even with its limitations, the human placental perfusion method provides information that can be used to evaluate the risk factors associated with drug use during pregnancy because understanding of specific transport characteristics is a good basis for rational risk assessment.
In conclusion, all of the tested in vitro systems were useful in the prediction of at least some aspects of in vivo pharmacokinetics and metabolism, but validation and refinement are still essential, as is also the need to keep in mind the limitations characteristic of each in vitro method.
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Deloison, Benjamin. "Imagerie fonctionnelle placentaire par résonance magnétique : étude de la perfusion placentaire". Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112256.
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L’insuffisance placentaire est une pathologie grave avec un diagnostic souvent trop tardif empêchant la mise en place de thérapeutiques efficaces. Le but de ce travail de Thèse est de développer chez la rate gestante et de transposer à l’Homme des outils d’IRM fonctionnelle (IRMf) placentaire qui permettrait une quantification de la perfusion placentaire en pratique clinique.Matériels et méthodes : Trois études en IRMf font partie de cette Thèse.Les deux premières ont été réalisées sur un modèle murin. Une séquence dynamique avec injection d’un agent de contraste (DCE) a été développée avec une particule de fer de type SPIO dans un modèle chirurgical d’hypoperfusion placentaire chronique, avec mesure de la perfusion placentaire f en ml/min/100ml et de la fraction volumique (Vb) en %. Une autre technique d’IRMf a été développée avec l’Arterial Spin Labeling (ASL) permettant d’estimer la perfusion placentaire en ml/min/100g sans injection de produit de contraste exogène. La dernière étude était une recherche translationnelle. Elle a consisté au développement de séquences de DCE avec injection de chélate de gadolinium, pour obtenir la perfusion f en ml/min/100ml et la fraction volumique en %. Nous avons également étudié, au décours de cette étude, la pharmacocinétique materno-fœtale du chélate de gadolinium.Résultats : Chez l’animal en DCE avec SPIO, notre étude nous a permis de montrer qu'il était possible d'utiliser l’effet T1 des SPIO pour caractériser la microcirculation placentaire par f=159,4 ml/min/100ml (+/- 54,6) et Vb =39,2% (+/- 11,9) pour 31 placentas « normaux ». En cas de RCIU, f diminue significativement pour les 23 placentas étudiés (f= 108,1 ml/min/100ml +/- 41, p=0,004), alors que la fraction volumique placentaire n'est pas modifiée (Vb=42,8% +/- 16,7, p=0,24). L’ASL nous a permis d’estimer la perfusion placentaire pour 47 placentas en condition physiologique, avec une perfusion estimée à 146,8 ml/min/100g (+/- 70,1).Chez l’Homme, 14 placentas ont été étudiés avec une perfusion placentaire globale estimée à 183 ml/min/100ml (+/-144) et nous avons également mis en évidence deux types de cinétique de rehaussement placentaire (précoce et intense et plus tardif et moins intense). La pharmacocinétique nous a permis d'étudier quantitativement le passage du chélate de gadolinium chez le fœtus. Ce passage est faible: par rapport à la concentration initiale du Dotarem®, la concentration sanguine fœtale correspond à 18,1x10-6 %, la concentration dans le liquide amniotique à 242,8 x10-6 % et 0,3 % de la dose initiale de Dotarem® est présente dans le placenta environ 70 heures après l’injection.Conclusion : Ce travail illustre la variété des techniques d'IRM fonctionnelle disponibles pour l'étude du placenta. La perfusion placentaire peut être quantifiée en DCE avec un agent particulaire à base de fer (SPIO) ou sans injection de produit de contraste en ASL chez le rat. L’étude de la perfusion placentaire chez l'Homme est possible en DCE avec les chélates de gadolinium.Mots clés : IRM, DCE, chélates de Gadolinium, ASL, perfusion placentaire, grossesse, placenta, retard de croissance intra-utérinPlacental insufficiency is a serious medical condition with a diagnosis made usually too late to prevent introduction of effective therapies. The aim of this thesis is to develop, in pregnant rats and translate to humans, functional MRI (fMRI) tools allowing quantification of placental perfusion in clinical practice.Materials and Methods: Three studies using fMRI are part of this thesis. The first two were performed on a murine model. A dynamic sequence with injection of a contrast agent (DCE) has been developed with an iron oxide particle (SPIO) in a surgical model of chronic placental hypoperfusion with placental perfusion measurement (f) in ml / min / 100 ml and placental fractionnal volume (Vb) in %. Another technique of fMRI was developed with Arterial Spin Labeling (ASL) to estimate placental perfusion in ml / min / 100g without injection of contrast media.The latest study was a translational research. It consisted in the development of a dynamic sequence with injection of gadolinium chelate, in order to obtain perfusion (f) in ml / min / 100 ml and placental fractionnal volume (Vb) in %. We also studied maternal and fetal pharmacokinetics of gadolinium chelate.Results: In animals with SPIO DCE, our study allowed us to show that it is possible to use the T1 effect of SPIO to characterize the placental microcirculation by f = 159.4 ml / min / 100ml (+ / - 54.6) and Vb = 39.2% (11.9 +/-) for 31 « normal » placentas. In case of IUGR, f decreases significantly for the 23 examined placentas (f = 108.1 ml / min / 100ml +/- 41, p = 0.004), whereas the volume fraction placenta is not modified (Vb = 42 +/- 16.7 8 %, p = 0.24). ASL has allowed us to estimate placental perfusion for 47 placentas under physiological conditions, with an estimated perfusion of 146.8 ml / min / 100 g (70.1 +/-).In humans, 14 placentas were studied with an estimated perfusion of 183 ml / min / 100ml (+/- 144) and we also identified two types of placental kinetic enhancement (early and intense and later and less intense). Pharmacokinetics have allowed us to study quantitatively the transfer of gadolinium chelate in the fetus. This transfer is low compared to the initial concentration of Dotarem® : fetal blood concentration is 18.1x10-6%, concentration in amniotic fluid is 242.8 x10-6 % and 0.3% of the Dotarem® initial dose is present in the placenta approximately 70 hours after injection.Conclusion: This study illustrates the variety of functional MRI techniques available for placental study. Placental perfusion can be quantified by DCE with an iron oxide particle (SPIO) or without injection of contrast in ASL, in a rat model. The study of placental perfusion in humans is also possible in DCE with gadolinium chelates
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Arthuis, Chloé. "Etude de la perfusion placentaire par imagerie fonctionnelle sur un modèle murin de retard de croissance intra-utérin". Thesis, Tours, 2016. http://www.theses.fr/2016TOUR3308.
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La distinction entre les fœtus constitutionnellement petits de ceux qui présentent une réelle restriction de croissance liée à une insuffisance placentaire n’est pas aisée avec les mesures échographiques utilisées en pratique courante. Le retard de croissance intra-utérin (RCIU) est responsable d’une part importante de la prématurité induite, et d’une augmentation du risque de mortalité et de morbidité néonatales. C’est pourquoi, l’amélioration de la connaissance de la vascularisation placentaire est indispensable pour mieux identifier et prendre en charge les situations d’hypoxie chroniques foetales associées à l’insuffisance placentaire.Pour quantifier la vascularisation les modalités d’imagerie de perfusion disponibles sont l’échographie et l’IRM. Les études évaluant la quantification de la perfusion placentaire par échographie de contraste sont peu nombreuses. Les avantages et les limites de cet examen ont été évalués sur un modèle murin de RCIU par ligature vasculaire. Ainsi, l’échographie de contraste permettait de quantifier une baisse de la perfusion placentaire sur un modèle de RCIU sans que l’on puisse observer de passage d’agents de contraste ultrasonores au travers la barrière placentaire. Les résultats obtenus ont été comparés aux données obtenues par l’IRM de perfusion. Les paramètres quantitatifs obtenus à partir des courbes de cinétiques du contraste pour chacune des deux modalités d’imagerie étaient comparables sur un modèle identique de RCIU murin. Enfin, une méthode d’étude de l’oxygénation placentaire par imagerie photoacoustique a été évaluée. Cette modalité d’imagerie non invasive permettait d’obtenir en temps réel l’oxygénation placentaire, avec cependant une profondeur limitée d’exploration. Le placenta semblait se comporter comme une réserve en oxygène au cours de l’étude d’une séquence hypoxie – hyperoxygénation maternelle avec une désaturation moins importante que celle observée dans les autres tissus maternelsTo identify fetuses small for their gestational-age who have reached their appropriate growth potential from growth-restricted fetuses due to placental insufficiency is uneasy. Intra Uterine Growth Restriction (IUGR) increases the risk for indicated preterm delivery, neonatal mortality and morbidity. Therefore, improving the knowledge of the placental perfusion is essential to better identify and manage fetal chronic oxygen deprivation associated with placental insufficiency.Contrast Enhanced Ultrasound (CEUS) and MRI are two imaging modalities available to quantify placental perfusion. However, few studies focus on the quantification of placental perfusion with CEUS. First, the advantages and limitations of CEUS were presented in an IUGR rat model by uterine ligation. The placental perfusion observed by CEUS was significantly decreased in the ligated horn. No contrast enhancement was observed in the umbilical vein or the fetus. Then, we compared the CEUS parameters to results obtained by MRI perfusion. Perfusion parameters were obtained from the signal intensity decay curve for the two imaging modalities. Results of such perfusion parameters were comparable in the same IUGR rat model. Finally, we evaluated the response of the placenta to oxygenation by photoacoustic imaging. PA imaging is a real-time, non-invasive method to evaluate placental oxygenation without contrast agents. Our results suggesting that placenta is less affected than maternal tissue by the decline in maternal oxygenation. The placenta may play an important role in protecting the feus against hypoxia
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Sohlberg, Sara. "Placental Function : An Epidemiological and Magnetic Resonance Study". Doctoral thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-239294.
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Placental function is central for normal pregnancy and in many of the major pregnancy disorders. We used magnetic resonance imaging techniques to investigate placental function in normal pregnancy, in early and late preeclampsia and in intrauterine growth restriction. We also investigated maternal body mass index and height, as risk factors for preeclampsia. A high body mass index and a short maternal stature increase the risk of preeclampsia, of all severities. The association seems especially strong between short stature and early preeclampsia, and a high body mass index and late preeclampsia. (Study I) Using diffusion-weighted magnetic resonance imaging, we found that the placental perfusion fraction decreases with increasing gestational age in normal pregnancy. Also, the placental perfusion fraction is smaller in early preeclampsia, and larger in late preeclampsia, compared with normal pregnancies. That these differences are in opposite directions, suggests that there are differences in the underlying pathophysiology of early and late preeclampsia. (Study II) Using magnetic resonance spectroscopy, we found that the phosphodiester spectral intensity fraction and the phosphodiester/phosphomonoester spectral intensity ratio increases with increasing gestational age. Also, we found that the phosphodiester spectral intensity fraction and the phosphodiester/phosphomonoester spectral intensity ratio are higher in early preeclampsia, compared with early normal pregnancy. These findings indicate increased apoptosis with increasing gestational age in normal pregnancy, and increased apoptosis in early preeclampsia. (Study III) The placental perfusion fraction is smaller in intrauterine growth restriction than in normal pregnancy. Fetal growth, Doppler blood flow in maternal and fetal vessels, infant birth weight and plasma markers of placental function are all correlated to the placental perfusion fraction. The placental perfusion fraction examination seems therefore to offer a fast, direct estimate of the degree of placental dysfunction. (Study IV) In conclusion: Our findings in studies I-III all support the hypothesis of partly different pathophysiology between early and late preeclampsia, and suggest a strong link between early preeclampsia and placental dysfunction. Study IV shows that the placental perfusion fraction has potential to contribute to the clinical assessment of placental dysfunction.
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Ceccaldi-Carp, Pierre-François. "Médicaments et parturition humaine : influences réciproques". Thesis, Paris 11, 2012. http://www.theses.fr/2012PA114851.
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L’étude du retentissement d’un xénobiotique en général ou d’un médicament en particulier sur la gestation humaine est difficile à appréhender. Elle doit prendre en compte des considérations éthiques, indispensables lors de toute recherche chez la femme enceinte, mais aussi pour le cas de l’induction de la parturition, de la complexité des mécanismes physiologiques impliqués. S’il existe un relatif consensus expérimental à partir de modèles animaux pour évaluer leur retentissement sur la fertilité et l’embryogenèse, il n’y a pas à ce jour d’attitude pour évaluer un risque induit d’un accouchement prématuré. Hors la naissance prématurée est la première cause de mortalité du nouveau-né et concerne quinze millions de naissances par an au niveau mondial. Les étiologies sont multiples : infectieuses dont VIH,grossesses multiples, addictions. La littérature récente fait part aussi de cette problématique pour certains médicaments indispensables comme les inhibiteurs de protéase chez les femmes enceintes infectées par le VIH. Nous avons réalisé trois études spécifiquement chez la femme enceinte : modulation du passage placentaire des inhibiteurs de protéase du VIH, modulation des hormones stéroïdiennes placentaires et materno-foetales par la mifépristone, variation des protéines sériques maternelles dans les jours précédents la parturition. C’est à l’issue de ces travaux que nous émettons plusieurs hypothèses sur l’incidence d’un médicament lors de la parturition humaine et les moyens envisagés pour l’étudier de manière la moins invasive possibleEffects of a xenobiotic or drug on human gestation are difficult to approach. This is due tonecessary ethical considerations with regards to research on pregnant women as well as thecomplexity of physiological processes involved in the case of induced parturition. While thereis a relative experimental consensus with animal models to assess their impact on fertility andembryogenesis, there is currently no method to assess the risk of induced preterm labor.Preterm labor is the leading cause of newborn deaths at the rate fifteen million births per yearglobally. The etiologies are multiple: infectious including HIV, multiple pregnancies,addictions. Recent publications also discuss this issue in the context of necessary drugs suchas protease inhibitors for HIV infected pregnant women. We realised three studies specificallyin pregnant women: modulation of the placental transfer of protease inhibitors of the HIV,modulation of the feto-maternal and placental steroid hormones by mifepristone, and a studyabout variation of the maternal serum proteins in the previous days of the parturition. Also,regarding our studies and the literature, we make several hypotheses on possible interferencesbetween drugs and human parturition, disturb its signal, and methods proposed for its study ina minimally invasive manner
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Aughwane, Rosalind Janie. "Investigating perfusion of the human placenta". Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10060708/.
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Placental insufficiency is a significant cause of morbidity and mortality, accounting for one third of antenatal stillbirths. It occurs when the maternal spiral arteries fail to remodel normally in early pregnancy, leading to inadequate maternal perfusion of the placenta. The fetus becomes hypoxic and if not delivered prematurely may ultimately die. Assessing the placenta is therefore clinically important, to diagnose placental insufficiency in vivo, and investigate poor pregnancy outcome ex vivo. Ex vivo placental assessment relies on subjective histological analysis of a small proportion of the placenta, looking for features such as oedema, inflammation and the presence of avascular villi. Regional variation and heterogeneity are not defined. In utero clinical assessment is via ultrasound Doppler measurements, looking for increased resistance in the uterine arteries, suggesting poor spiral artery remodeling, and increased resistance within the umbilical artery, suggesting inadequate development of the feto-placental microcirculation. There is therefore an urgent need to develop new ways to evaluate the perfusion of the placenta both in and ex vivo. In this thesis I investigate two imaging modalities with the potential to improve our understanding of placental perfusion. Ex vivo I develop a placental perfusion and micro-CT imaging technique, to directly visualise the feto-placental microcirculation, before applying the technique to investigate heterogeneity within a cohort of normal term placentae. I investigate differences in vascular density through the placenta at multiple scales. In vivo I investigate a novel Magnetic Resonance Imaging model of placental perfusion, that combines diffusion weighted imaging with T2 relaxometry, to estimate maternal and fetal placental perfusion. I develop this technique, exploring MRI parameters relating to perfusion in normally grown and growth restricted pregnancies. This work is important as the techniques developed improve our ability to investigate and understand placental perfusion, and provide potential new parameters of placental function in vivo.
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Alison, Marianne. "Imagerie fonctionnelle du placenta en IRM". Thesis, Paris 11, 2012. http://www.theses.fr/2012PA112329.
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L’insuffisance placentaire par défaut de vascularisation est une pathologie fréquente de la grossesse, de diagnostic difficile, avec des complications potentiellement graves (retard de croissance intra utérin, prééclampsie). L’objectif de ce travail de Thèse a été de développer l’IRM fonctionnelle multiparamétrique pour l’exploration du placenta à 4.7 T chez la rate gestante. Matériel et méthode : L’IRM de diffusion (SE- EPI DWI) avec analyse IVIM et l’IRM dynamique avec injection de gadolinium (DCE) et haute résolution temporelle (< 1s) ont été développées puis étudiées sur un modèle murin contrôlé d’hypoperfusion placentaire par ligature du pédicule vasculaire utérin gauche au 17ème jour de gestation. Les paramètres obtenus sur les placentas hypoperfusés de la corne gauche ligaturée étaient comparés à ceux des placentas normaux de la corne droite. L’effet de l’hyperoxygénation maternelle était étudié en diffusion. Résultats : Ont été étudiés 73 placentas, dont 23 pathologiques (n= 10 rates) en diffusion et 53 placentas, dont 11 pathologiques (n=12 rates) en DCE. Les paramètres significativement diminués du côté hypoperfusé étaient le coefficient apparent de diffusion (ADC), la fraction de perfusion (f) en diffusion et le flux sanguin maternel (F) en DCE. Sous hyperoxygénation maternelle, l’ADC et le coefficient de diffusion (D) augmentaient et f diminuait. Les paramètres obtenus en diffusion et en DCE n’étaient pas nettement corrélés entre eux. Conclusion : Un outil d’IRM fonctionnelle placentaire multiparamétrique a été développé à 4.7 T chez la rate gestante. La DWI comme la DCE apparaissent complémentaires pour le diagnostic d’hypoperfusion placentairePlacental insufficiency caused by deficient vascularization is common during pregnancy, difficult to diagnose and can lead to severe materno-fetal complications (intrauterine growth restriction, preeclampsia). The aim of this work was to develop multi-parametric functional magnetic resonance imaging (MRI) to assess the placenta at 4.7 T on a murine model. Materials and methods : Diffusion-weighted imaging (SE-EPI-DWI) with the intravoxel incoherent motion (IVIM) analysis and dynamic contrast enhanced MRI (DCE) with a high-time resolution (<1 s) were developed and evaluated on a controlled rat model of reduced placental perfusion, achieved by ligation of the left uterine vascular pedicle on the 17th embryonic day. Parameters from the placentas in the left ligated horn were compared to those from the normal placentas in the non ligated horn. The effect of maternal hyperoxygenation on placental microvascularization was studied with DWI.Results: For DWI, 73 placentas were examined, 23 from the ligated side (n=10 rats). For DCE, 53 placentas were analysed, 11 from the ligated side (n=12 rats). In the uterine horn with reduced perfusion, the apparent diffusion coefficient (ADC), the perfusion fraction (f) obtained with DWI and the placental blood flow (F) obtained with DCE were significantly decreased. Under maternal hyperoxygenation, ADC and the diffusion coefficient (D) increased whereas f decreased. DWI and DCE parameters were not significantly correlated with each other. Conclusion: Multi-parametric MRI has been developed for murine placental analysis at 4.7T. DWI and DCE are complementary tools for the diagnosis of reduced placental perfusion
Książki na temat "Placental perfusion"
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(Editor), J. Dancis, red. In Vitro Perfusion of Human Placental Tissue (Contributions to Gynecology and Obstetrics). S. Karger AG (Switzerland), 1986.
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Bonnet, Marie-Pierre, i Anne Alice Chantry. Placenta and uteroplacental perfusion. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0003.
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The placenta is a complex and changing organ necessary for normal fetal growth and development and for maintenance of a healthy pregnancy. It has three major functions: a protective function of the fetus, an endocrine function, and a metabolic function. The main functional unit of the placenta is the chorionic villous, responsible for the majority of the fetal–maternal exchanges. Migration of trophoblastic cells induces a remodelling of the uterine arteries, with vasodilatated and compliant vessels, unresponsive to maternal vasomotor control. Therefore, any significant change in maternal blood pressure, in particular in the context of general or regional anaesthesia, can directly impact on uteroplacental perfusion. Most anaesthetic drugs cross the placental barrier, but without significant consequences on the fetal well-being.
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Schneider, H., i J. Dancis, red. In vitro Perfusion of Human Placental Tissue. S. Karger AG, 1985. http://dx.doi.org/10.1159/isbn.978-3-318-03236-9.
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Waldmann, Carl, Neil Soni i Andrew Rhodes. Obstetric emergencies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0031.
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Pre-eclampsia 518Eclampsia 520HELLP syndrome 522Postpartum haemorrhage 524Amniotic fluid embolism 526Pre-eclampsia is a common complication of pregnancy, UK incidence is 3–5%, with a complex hereditary, immunological and environmental aetiology.Abnormal placentation is characterized by impaired myometrial spiral artery relaxation, failure of trophoblastic invasion of these arterial walls and blockage of some vessels with fibrin, platelets and lipid-laden macrophages. There is a 30–40%, reduction in placental perfusion by the uterine arcuate arteries as seen by Doppler studies at 18–24 weeks gestation. Ultimately the shrunken, calcified, and microembolized placenta typical of the disease is seen. The placental lesion is responsible for fetal growth retardation and increased risks of premature labour, abruption and fetal demise. Maternal systemic features of this condition are characterized by widespread endothelial damage, affecting the peripheral, renal, hepatic, cerebral, and pulmonary vasculatures. These manifest clinically as hypertension, proteinuria and peripheral oedema, and in severe cases as eclamptic convulsions, cerebral haemorrhage (the most common cause of death due to pre-eclampsia in the UK), pulmonary oedema, hepatic infarcts and haemorrhage, coagulopathy and renal dysfunction....
Części książek na temat "Placental perfusion"
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Pateisky, N. "Clonidine and Placental Perfusion". W Low Dose Oral and Transdermal Therapy of Hypertension, 126–28. Heidelberg: Steinkopff, 1985. http://dx.doi.org/10.1007/978-3-642-53785-1_25.
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Maguire, D. J., G. R. Cannell, R. S. Addison i B. Dawkins. "In Vitro Placental Perfusion". W Advances in Experimental Medicine and Biology, 361–66. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4717-4_43.
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Maguire, D. J., R. Blums, R. Morgan, J. Collie i G. R. Cannell. "A Placental Perfusion pO2 Logger". W Oxygen Transport to Tissue XIV, 649–52. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3428-0_77.
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Slikker, William, John R. Bailey, George W. Lipe, Zelda Althaus i Julian E. A. Leakey. "Placental Steroid Dehydrogenases: Assessment with a Nonhuman Primate in Situ Placental Perfusion Model". W Cellular Biology and Pharmacology of the Placenta, 467–79. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-1936-9_33.
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Anthony di Sant’Agnese, P., Karen L. de Mesy Jensen, Patrick J. Wier, Debabrata Maulik i Richard K. Miller. "Long Term Human Placental Lobule Perfusion — An Ultrastructural Study". W Cellular Biology and Pharmacology of the Placenta, 545–55. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-1936-9_39.
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Aughwane, Rosalind, Magdalena Sokolska, Alan Bainbridge, David Atkinson, Giles Kendall, Jan Deprest, Tom Vercauteren, Anna L. David, Sébastien Ourselin i Andrew Melbourne. "MRI Measurement of Placental Perfusion and Fetal Blood Oxygen Saturation in Normal Pregnancy and Placental Insufficiency". W Medical Image Computing and Computer Assisted Intervention – MICCAI 2018, 913–20. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-00934-2_101.
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Howard, Randy B., Janet Levy, Tomokazu Hosokawa i M. Helen Maguire. "Interrelationships of Perfusion Parameters in the Dual-Perfused Human Placental Cotyledon". W Cellular Biology and Pharmacology of the Placenta, 585–96. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-1936-9_42.
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Schneider, H., A. Malek, R. Duft i N. Bersinger. "Evaluation of an In Vitro Dual Perfusion System for the Study of Placental Proteins: Energy Metabolism". W Placenta as a Model and a Source, 39–50. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0823-2_4.
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Myatt, Leslie. "Perfusion Technique for Studying the Placenta Cotyledon". W The Placenta, 170–76. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444393927.ch22.
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Schneider, Henning, i Joseph Dancis. "In Vitro Perfusion of Human Placenta". W Cellular Biology and Pharmacology of the Placenta, 597–605. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-1936-9_43.
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Novell, Anthony, Vanda Mendes, Arthuis Chloe, Ayache Bouakaz i Franck Perrotin. "Notice of Removal: Evaluation of utero-placental perfusion in intrauterine growth restriction rat model using CEUS". W 2017 IEEE International Ultrasonics Symposium (IUS). IEEE, 2017. http://dx.doi.org/10.1109/ultsym.2017.8092965.
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Fernandes, Karol Arias, Emily Nefertiti Balbinot, Emmanuela Regina Silveira i Leslie Ecker Ferreira. "INTERAÇÃO ENTRE SARS-COV-2 E A GESTAÇÃO HUMANA: UMA REVISÃO LITERÁRIA". W I Congresso On-line Nacional de Histologia e Embriologia Humana. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/rems/3209.
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Introdução: O vírus SARS-CoV-2 foi responsável pela pandemia iniciada em 2020 e com alto impacto para a saúde pública mundial. Grandes esforços científicos estão sendo realizados para uma melhor compreensão do mecanismo patogênico da doença em humanos. Sabe-se que há repercussões diretas e indiretas sobre a saúde reprodutiva da mulher, no entanto ainda são escassos os estudos com forte associação entre a viremia e a gestação. Objetivos: Realizar uma revisão de literatura a fim de analisar a interação entre SARS-CoV-2 e a gestação humana. Material e métodos: Trata-se de um estudo de revisão de literatura, onde a busca dos artigos ocorreu nas bases de dados Pubmed e Scielo publicados entre outubro de 2020 e dezembro de 2021. Utilizou-se os descritores: “gestação (pregnancy)” e “COVID-19” com o operador booleano “AND”. Como critérios de exclusão foram descartados os artigos que não atenderam ao objetivo do estudo e de texto completo não disponível. Dos trinta e três artigos encontrados, foram incluídos nesta revisão 10 artigos. Resultados: Apesar do quadro clínico não diferir no caso de gestação, as modificações fisiológicas no período gravídico (principalmente relacionadas a mecânica respiratória), justificam os dados epidemiológicos que demonstram uma maior vulnerabilidade durante esse período. Quanto à transmissão vertical, a análise da placenta é essencial para o diagnóstico. Assim, apesar da incerteza quanto à relevância dos seguintes achados, estudos encontraram evidências de má perfusão vascular ou trombose vascular na circulação fetal na análise de placentas. Conclusão: Diante disso, é perceptível a necessidade de mais estudos acerca do tema, uma vez que os dados alertaram números elevados de morte materna e as pesquisas ainda são preliminares, assim como também é reconhecível a importância da implementação do protocolo de coleta placentária para elucidar aspectos críticos da infecção por SARS-CoV-2.