Blood Flow Regulation in the Uteroplacental Arteries

Moll, W.; Nienartowicz, Andrzej; Hees, Herbert; Wrobel, Karl‐Heinz; Lenz, Andreas

doi:10.1007/978-1-4615-8109-3_7

Cited by 13 publications

(12 citation statements)

References 18 publications

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“…In PE patients, these vessels undergo minor modifications, with apparent substitution of the media layer cells by invasive trophoblasts, increased apoptosis of trophoblast cells, placental ischemia and loss of vasomotor control. Our results are consistent with the findings of other authors (Moll, Nienartowicz, Hees, Wrobel, & Lenz, 1988;Zhou, Damsky, & Fisher, 1997;Rein et al, 2003;Roberts & Gammill, 2005;Benirschke, Kaufmann, & Baergen, 2006).…”

Section: Immunohistochemistry (Ihc)supporting

confidence: 94%

<b>Expression of bradykinin in human placenta from healthy and preeclamptic women

Oliveira

Pereira

Bertevello

et al. 2017

Acta Sci. Health Sci.

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ABSTRACT. This study evaluated the expression of bradykinin (BK) in human placenta from healthy and preeclamptic women. This is a non-randomized experimental study, in which we performed histological analysis of placental tissue to observe changes that occur in each kind of placenta as well as immunohistochemical analysis to investigate the expression of bradykinin. We used 'Paleontological Statistics software package for education and data analysis' 3.06 and R for the statistical analysis. The Ethics Committee of the University of Rio Grande do Norte State approved this experiment under protocol number 166370, according to the determinations established by Resolutions 466/12 and 441/11.We found differences between the two kinds of placenta concerning the diameter of the vessels and the rate of cytotrophoblastic invasion. Student's t-test evidenced significant difference (p = 7.6395 x 10 -5 ) indicating greater marking of BK per section in the healthy placenta group. The result of more significant expression of bradykinin in healthy placenta can be used as a starting point for deeper researches aiming to better characterize and quantify this expression.Keywords: gynecology, obstetrics, immunohistochemistry.Expressão de bradicinina em placentas humanas saudáveis e pré-eclâmpticas RESUMO. Este estudo avaliou a expressão de bradicinina em placentas humanas saudáveis e pré-eclâmpticas. Trata-se de um estudo de caráter experimental não randomizado, no qual foi feita uma análise histológica dos tecidos placentários, permitindo a observação das alterações ocorridas em cada tipo de placenta, e a técnica de imuno-histoquímica, a fim de investigar a presença de bradicinina. Foi utilizado o Paleontological Statistics software package for education and data analysis 3.06 para a análise estatística. Este estudo foi aprovado pelo Comitê de Ética da Universidade do Estado do Rio Grande do Norte sob o protocolo número 166.370, de acordo com as diretrizes estabelecidas nas Resoluções 466/12 e 441/11. Foi possível observar diferenças no diâmetro dos vasos e na invasão citotrofoblástica entre os dois tipos de placentas. O teste t de Student mostrou significância estatística (p = 7,6395 x 10 -5 ) para uma maior marcação de BK por secção no grupo de placentas saudáveis. O resultado obtido com relação à expressão mais significante de bradicinina em placentas saudáveis pode ser visto como precursor de uma pesquisa mais aprofundada, para melhor caracterizar e quantificar essa expressão.Palavras-chave: ginecologia, obstetrícia, imuno-histoquímica.

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Section: Immunohistochemistry (Ihc)supporting

confidence: 94%

<b>Expression of bradykinin in human placenta from healthy and preeclamptic women

Oliveira

Pereira

Bertevello

et al. 2017

Acta Sci. Health Sci.

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“…To the best of our knowledge, the control of the 'well-known pregnancy-induced arterial dilation upstream' by trophoblast invasion of the spiral arteries has not yet been sufficiently explained. In guinea pig experiments, Moll et al 16 showed that prior to trophoblast invasion, oestrogens might have already stimulated vessel growth and dilatation. However, the more likely explanation for our findings of comparable flows per square unit proximal arterial cross section in AGA and IUGR is that arterial width of the upstream segments of the uterine arteries only secondarily adapts to the flow requirements defined by trophoblast invasion and dilatation of the downstream segments (spiral arteries).…”

Section: Discussionmentioning

confidence: 99%

Longitudinal quantification of uterine artery blood volume flow changes during gestation in pregnancies complicated by intrauterine growth restriction

Konje¹

2003

BJOG: An International Journal of Obstetrics and Gynaecology

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. Volume flow in the IUGR group was 12.5% and 36.7% less than that in the AGA group at 20 and 28 weeks of gestation, respectively. Conclusion Proximal uterine artery diameter and quantified volume flow change with gestation and show significant differences between AGA pregnancies and those complicated by IUGR. These changes occur early and become more marked as pregnancy advances. Early use of these measurements may identify pregnancies at risk of complications.

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“…72, 73, 111, 112), since its injection results in both acute and chronic increases in uterine blood flow related to vasodilation and increased cardiac output (19), and its in vitro application to isolated vessels induces vasorelaxation, albeit in concentrations that are several orders of magnitude higher than those present in vivo. Daily injections of estradiol benzoate (7–11 µg) for 3 wk induced a greater than twofold increase in the internal diameter of segmental mesometrial arteries of ovariectomized guinea pigs (85). Exogenous estradiol treatment in guinea pigs also stimulated DNA synthesis within the uterine artery (74) and increased cellular responsiveness to growth factors such as platelet-derived growth factor (PDGF) by a PKC-dependent mechanism (57).…”

Section: Mechanisms Underlying Gestational Uterine Vascular Remodelingmentioning

confidence: 99%

Maternal Uterine Vascular Remodeling During Pregnancy

2009

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This classification was proposed by Mulvany (86) and is further refined to include consideration of wall mass, which can increase (hypertrophy), decrease (hypotrophy), or remain unchanged (eutrophy). Various patterns of arterial remodeling are shown in FIGURE 1; see legend for additional detail and for consideration of how changes in crosssectional area, a two-dimensional quantity (e.g., m 2 ), relate to changes in wall mass, a three-dimensional quantity (e.g., m 3 ). Uterine Hemodynamics DuringPregnancy; Blood Flow Patterns and the Importance of Placentation Type Uterine vascular anatomyAn overview of comparative uterine vascular anatomy is presented in FIGURE 2, which describes and illustrates the uterine circulation in humans (FIGURE 2A), rodents (FIGURE 2B), and ungulates, such as sheep and pigs. Please see legend for additional detail.Uterine and placental blood flow during pregnancy Early (1953Early ( -1960 human studies by Assali et al (3, 4) and Metcalfe (78) utilizing the diffusion equilibrium principle (most often nitrous oxide, N 2 O) or electromagnetic flow probes placed directly on the uterine artery reported that total uteroplacental blood flow (UPBF) increases from a baseline value of 20-50 ml/min to 450-800 ml/min in singleton pregnancies, with values in excess of 1 l/min measured in twin pregnancy. Subsequent measurements of uterine artery blood flow with 133 Xe (106), placental metabolic clearance rate techniques (29) The clinical relevance of maternal uterine vascular adaptation during pregnancy is underscored by the fact that its aberrance is associated with several common gestational pathologies, including intrauterine growth restriction, gestational diabetes, and preeclampsia.In addition to the changes in vessel structure, uterine vascular reactivity is also altered during pregnancy, with the general pattern being one of reduced tone and enhanced vasodilation/blunted vasoconstriction (52,72,111,112,118). Space limitations preclude indepth consideration of the ionic and enzymatic mechanisms that underlie reactivity, but it is worth noting that, in vivo, uterine vascular resistance (and, therefore, blood flow) is ultimately determined by the combination of vessel size and reactivity.We also avoid examining the complex angiogenic mechanisms associated with implantation and placentation, other than to consider how hemochorial vs. epitheliochorial placentation influences uterine hemodynamics and vascular remodeling. Although the remodeling of spiral arteries by fetal trophoblast is considered, the main focus of this review is on upstream maternal uterine arteries and veins, since the processes involved in their remodeling have not been reviewed to date. Readers interested in endovascular trophoblast invasion and mechanisms underlying spiral artery remodeling are referred to several reviews on this subject (9, 31, 71, 101). Nomenclature Used to Describe Vascular RemodelingCircumferential remodeling is normally termed inward or outward to denote narrowing vs. widening of the vessel lumen. The ...

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Blood Flow Regulation in the Uteroplacental Arteries

Cited by 13 publications

References 18 publications

<b>Expression of bradykinin in human placenta from healthy and preeclamptic women

<b>Expression of bradykinin in human placenta from healthy and preeclamptic women

Longitudinal quantification of uterine artery blood volume flow changes during gestation in pregnancies complicated by intrauterine growth restriction

Maternal Uterine Vascular Remodeling During Pregnancy

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