Permeability of the human placenta in vivo to four non‐metabolized hydrophilic molecules.

Bain, Murray D.; Copas, D K; Taylor, Alison R.; Landon, Michael; Stacey, T. E.

doi:10.1113/jphysiol.1990.sp018343

Cited by 44 publications

(27 citation statements)

References 22 publications

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“…The main evidence for such channels is that the human placenta is freely permeable to solutes of 1350-5200 daltons, whereas in the epitheliochorial placenta of the sheep diffusion is restricted to molecules of more than 400 daltons [13,14]. By measuring the transplacental flux of four permeants of different molecular sizes infused into patients prior to elective caesarean section, it was concluded that pores of different sizes must exist in the human syncytiotrophoblast [15]. However, the putative channels have never been visualized in the human [16], although this lack may reflect the complexity of the syncytioplasm and the limitations of current imaging techniques.…”

Section: Placental Transportmentioning

confidence: 99%

The placenta: a multifaceted, transient organ

Burton

Fowden

2015

Phil. Trans. R. Soc. B

575

380

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The placenta is arguably the most important organ of the body, but paradoxically the most poorly understood. During its transient existence, it performs actions that are later taken on by diverse separate organs, including the lungs, liver, gut, kidneys and endocrine glands. Its principal function is to supply the fetus, and in particular, the fetal brain, with oxygen and nutrients. The placenta is structurally adapted to achieve this, possessing a large surface area for exchange and a thin interhaemal membrane separating the maternal and fetal circulations. In addition, it adopts other strategies that are key to facilitating transfer, including remodelling of the maternal uterine arteries that supply the placenta to ensure optimal perfusion. Furthermore, placental hormones have profound effects on maternal metabolism, initially building up her energy reserves and then releasing these to support fetal growth in later pregnancy and lactation post-natally. Bipedalism has posed unique haemodynamic challenges to the placental circulation, as pressure applied to the vena cava by the pregnant uterus may compromise venous return to the heart. These challenges, along with the immune interactions involved in maternal arterial remodelling, may explain complications of pregnancy that are almost unique to the human, including pre-eclampsia. Such complications may represent a trade-off against the provision for a large fetal brain.

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Section: Placental Transportmentioning

confidence: 99%

The placenta: a multifaceted, transient organ

Burton

Fowden

2015

Phil. Trans. R. Soc. B

575

380

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“…Passive diffusion makes a quantitatively significant contribution to fluxes of all solutes across the placenta (10)(11)(12). In the human, up to 50% of the unidirectional flux of, for example, ions is via diffusion (12), and therefore any decrease in the passive permeability of the placenta to hydrophilic nutrients will have a significant impact on total transfer capacity and therefore fetal growth potential.…”

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confidence: 99%

Placental-specific insulin-like growth factor 2 ( Igf2 ) regulates the diffusional exchange characteristics of the mouse placenta

Sibley

Coan

Ferguson-Smith

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

291

216

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Restricted fetal growth is associated with postnatal mortality and morbidity and may be directly related to alterations in the capacity of the placenta to supply nutrients. We proposed previously that imprinted genes can regulate nutrient supply by the placenta. Here, we tested the hypothesis that the insulin-like growth factor 2 gene (Igf2) transcribed from the placental-specific promoter (P0) regulates the development of the diffusional permeability properties of the mouse placenta. Using mice in which placental-specific Igf2 had been deleted (P0), we measured the transfer in vivo of three inert hydrophilic solutes of increasing size ( 14 C-mannitol, 51 CrEDTA, and 14 C-inulin). At embryonic day 19, placental and fetal weights in P0 conceptuses were reduced to 66% and 76%, respectively, of wild type. In P0 mutants, the permeability⅐surface area product for the tracers at this stage of development was 68% of that of controls; this effect was independent of tracer size. Stereological analysis of histological sections revealed the surface area of the exchange barrier in the labyrinth of the mouse placenta to be reduced and thickness increased in P0 fetuses compared to wild type. As a result, the average theoretical diffusing capacity in P0 knockout placentas was dramatically reduced to 40% of that of wild-type placentas. These data show that placental Igf2 regulates the development of the diffusional exchange characteristics of the mouse placenta. This provides a mechanism for the role of imprinted genes in controlling placental nutrient supply and fetal growth. Altered placental Igf2 could be a cause of idiopathic intrauterine growth restriction in the human.

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“…Furthermore, a long list of chronic diseases are associated with specific placental phenotypes. 27 The transport of required nutrients from mother to fetus requires optimal function of a myriad of separate transport mechanisms including 1) diffusional permeability to blood gases, 28–31 2) transporters facilitating diffusion of glucose and fatty acids, 32,33,34 3) active transporters for amino acids and some ions, 34–36 4) vesicular transport systems that regulate the transport of iron and immunoglobulins and many others. 37,38 Thus, each of these processes are known to be, or thought to be, associated with compromised fetal growth.…”

Section: The Placenta As Culpritmentioning

confidence: 99%

The placenta is the center of the chronic disease universe

Thornburg

Marshall

2015

American Journal of Obstetrics and Gynecology

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Over the past quarter century it has become clear that adult onset chronic diseases like heart disease and type 2 diabetes have their roots in early development. The report by David Barker and colleagues showing an inverse relationship between birthweight and mortality from ischemic heart disease was the first clear-cut demonstration of fetal programming. Because fetal growth depends upon the placental capacity to transport nutrients from maternal blood, it has been a suspected causative agent since the original Barker reports. Epidemiological studies have shown that placental size and shape have powerful associations with offspring disease. More recent studies have shown that maternal phenotypic characteristics, such as body mass index and height, interact with placental size and shape to predict disease with much more precision than does birthweight alone. For example, among people in the Helsinki Birth Cohort, who were born during 1924–1944, the risk for acquiring colorectal cancer increased as the placental surface became longer and more oval. Among people in whom the difference between the length and breadth of the surface exceeded 6 cm, the hazard ratio for the cancer was 2.3 (95% CI 1.2–4.7, p=0.003) compared with those in whom there was no difference. Among Finnish men, the hazard ratio for coronary heart disease was 1.07 (1.02–1.13, P =0.01) per 1% increase in the placental weight/birthweight ratio. Thus, it appears that the ratio of birthweight to placental weight, known as placental efficiency, predicts cardiovascular risk as well. Babies born with placentas at the extremes of efficiency are more vulnerable for adult onset chronic diseases. Recent evidence suggests that placental growth patterns are sex specific. Boys’ placentas are, in general, more efficient than those made by girls. Another recent discovery is that the size, shape and efficiencies of the placenta can change over years of time with very narrow confidence limits. This suggests that the growth of the placenta within a population of women is strongly affected by their nutritional environment. Even though it is known that an individual placenta can expand to improve its nutrient acquisition capacity in the first 2/3rd of gestation, the mechanisms by which placentas grow in response to a specific nutritional environment are not known. Discovering those mechanisms is the task of the current generation of scientists. While it may seem obvious that good nutrition is highly important for women who are pregnant because it supports optimal placentation and fetal development, more research is needed to determine the mechanisms by which maternal nutrition, placenta growth and fetal health are related.

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Permeability of the human placenta in vivo to four non‐metabolized hydrophilic molecules.

Cited by 44 publications

References 22 publications

The placenta: a multifaceted, transient organ

The placenta: a multifaceted, transient organ

Placental-specific insulin-like growth factor 2 ( Igf2 ) regulates the diffusional exchange characteristics of the mouse placenta

The placenta is the center of the chronic disease universe

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