Human Placental Vascularization

Leiser, Rudolf; Kosanke, G.; Kaufmann, Peter

doi:10.1159/000420847

Cited by 14 publications

(38 citation statements)

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“…However, their branching structure has been studied in some detail [7,8]. No existing model explicitly incorporates this structure.…”

Section: Villous Vesselsmentioning

confidence: 99%

“…These models have an advantage over models that represent an isolated subregion of the placenta, in that flow velocity waveforms can be measured in the umbilical vessels, and so boundary conditions defining pressure and flow in the umbilical vessels can be readily defined. However, because the placenta contains many thousands of blood vessels [7], the fluid dynamics of blood flow in the system, the geometry or both must be simplified to attain a computationally tractable model of the function of the system. In existing studies, the asymmetric structure of the placental vasculature is simplified to a symmetrically branching tree with 14-15 generations at term [28], or a single unit [29], and by solving for wave propagation through the system.…”

Section: System Modelsmentioning

confidence: 99%

“…Intraplacental vessels were generated to branch from the main chorionic arteries at the midpoint of each artery by refining each chorionic element once at its midpoint and generating an additional element oriented at 908 to its parent branch [4][5][6]36], extending 2 mm into the placenta [7]. A bifurcation between a chorionic vessel and an intraplacental vessel is shown in figure 3a.…”

Section: Chorionic Vesselsmentioning

confidence: 99%

“…In normal placentas, they branch in a mostly dichotomous manner to ultimately form approximately 60-100 chorionic arteries as small as 0.8 mm in diameter that branch into villous tissue [4][5][6]. As these vessels extend into the underlying villus tree, they branch further into multiple arterioles and venules that terminate in a dense network of capillary 'convolutes' [7][8][9]. In terms of temporal scale, the placenta is constantly developing throughout gestation, with significant blood flow in the feto-placental circulation at approximately eight weeks of gestation, and flow increasing through to term [10,11].…”

Section: Introductionmentioning

confidence: 99%

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Multiscale modelling of the feto–placental vasculature

et al. 2015

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One contribution of 11 to a theme issue 'Multiscale modelling in biomechanics: theoretical, computational and translational challenges'. The placenta provides all the nutrients required for the fetus through pregnancy. It develops dynamically, and, to avoid rejection of the fetus, there is no mixing of fetal and maternal blood; rather, the branched placental villi 'bathe' in blood supplied from the uterine arteries. Within the villi, the feto-placental vasculature also develops a complex branching structure in order to maximize exchange between the placental and maternal circulations. To understand the development of the placenta, we must translate functional information across spatial scales including the interaction between macro-and micro-scale haemodynamics and account for the effects of a dynamically and rapidly changing structure through the time course of pregnancy. Here, we present steps towards an anatomically based and multiscale approach to modelling the feto-placental circulation. We assess the effect of the location of cord insertion on feto-placental blood flow resistance and flow heterogeneity and show that, although cord insertion does not appear to directly influence feto-placental resistance, the heterogeneity of flow in the placenta is predicted to increase from a 19.4% coefficient of variation with central cord insertion to 23.3% when the cord is inserted 2 cm from the edge of the placenta. Model geometries with spheroidal and ellipsoidal shapes, but the same volume, showed no significant differences in flow resistance or heterogeneity, implying that normal asymmetry in shape does not affect placental efficiency. However, the size and number of small capillary vessels is predicted to have a large effect on feto-placental resistance and flow heterogeneity. Using this new model as an example, we highlight the importance of taking an integrated multi-disciplinary and multiscale approach to understand development of the placenta.

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“…However, their branching structure has been studied in some detail [7,8]. No existing model explicitly incorporates this structure.…”

Section: Villous Vesselsmentioning

confidence: 99%

Section: System Modelsmentioning

confidence: 99%

Section: Chorionic Vesselsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Multiscale modelling of the feto–placental vasculature

et al. 2015

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“…We have chosen to test placental stem villi small arteries in this study as these vessels are believed to contribute to the establishment of the foeto-placental resistance in man (Kaufmann, 1982;Leiser et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Endothelial modulation of vasoconstrictor responses to endothelin‐1 in human placental stem villi small arteries

Sabry

Mondon

Lévy

et al. 1995

British J Pharmacology

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1 The aim of this study was to assess the role of endothelial cells in the modulation of vasocontractile responses to endothelin-1 (ET-1) of human placental vasculature.2 Isolated stem villi small arteries (diameter = 170-250 gm) were obtained from healthy parturients who underwent caesarean surgery during the 39th week of pregnancy for cephalo-pelvic disproportion. Isometric tension was measured in vascular rings mounted in a myograph system and challenged with ET-1 (10-12 to 10-6 M). 3 The vasocontractile response to ET-1 was significantly (P<0.0001) increased in endothelial-denuded (active tension= 1156 + 214 mN mm-') as compared with endothelial-preserved vascular rings (active tension = 458 ± 48 mN mm-1). This difference was significantly (P< 0.05) but only partly abolished by the NO synthase inhibitor N1'-nitro-L-arginine (L-NOARG, 10' M).4 In endothelial-preserved rings submaximally precontracted with 5-hydroxytryptamine (10-6 M), ET-1 (10-12 to 10-9 M) induced dose-dependent relaxation (maximum relaxation = 70 + 7%) at 10-9 M, which was followed, at higher doses (10-8 to 10-6 M), by a contraction. In contrast, no relaxation was seen in endothelial-denuded rings. The relaxation in rings with endothelium was significantly (P<0.001) reduced by L-NOARG (10-4 M). Moreover, it was totally abolished by combined pretreatment with L-NOARG (10-4 M) and the sulphonylurea glibenclamide (10' M). 5 In conclusion, endothelial cells modulate the vascular responses to ET-1 through the release of NO and a substance acting on the ATP-sensitive K+ channel of smooth muscle of stem villi small arteries from healthy parturients.

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Computational modeling of the interactions between the maternal and fetal circulations in human pregnancy

Clark

Lee

James

2020

WIREs Mechanisms of Disease

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In pregnancy, fetal growth is supported by its placenta. In turn, the placenta is nourished by maternal blood, delivered from the uterus, in which the vasculature is dramatically transformed to deliver this blood an ever increasing volume throughout gestation. A healthy pregnancy is thus dependent on the development of both the placental and maternal circulations, but also the interface where these physically separate circulations come in close proximity to exchange gases and nutrients between mum and baby. As the system continually evolves during pregnancy, our understanding of normal vascular anatomy, and how this impacts placental exchange function is limited. Understanding this is key to improve our ability to understand, predict, and detect pregnancy pathologies, but presents a number of challenges, due to the inaccessibility of the pregnant uterus to invasive measurements, and limitations in the resolution of imaging modalities safe for use in pregnancy. Computational approaches provide an opportunity to gain new insights into normal and abnormal pregnancy, by connecting observed anatomical changes from high-resolution imaging to function, and providing metrics that can be observed by routine clinical ultrasound. Such advanced modeling brings with it challenges to scale detailed anatomical models to reflect organ level function. This suggests pathways for future research to provide models that provide both physiological insights into pregnancy health, but also are simple enough to guide clinical focus. We the review evolution of computational approaches to understanding the physiology and pathophysiology of pregnancy in the uterus, placenta, and beyond focusing on both opportunities and challenges.

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Human Placental Vascularization

Cited by 14 publications

References 0 publications

Multiscale modelling of the feto–placental vasculature

Multiscale modelling of the feto–placental vasculature

Endothelial modulation of vasoconstrictor responses to endothelin‐1 in human placental stem villi small arteries

Computational modeling of the interactions between the maternal and fetal circulations in human pregnancy

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