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cotyledon/hypoxia

Odkaz sa uloží do schránky
ČlánkyKlinické štúdiePatenty
6 výsledky

Fetoplacental vascular tone during fetal circuit acidosis and acidosis with hypoxia in the ex vivo perfused human placental cotyledon.

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OBJECTIVE Our purpose was to determine the effects of acidosis and acidosis-hypoxia on fetoplacental perfusion pressure and its response to angiotensin II. METHODS Perfused cotyledons from 14 placentas were studied with either an acidotic fetal circuit perfusate (n = 7) or an acidotic-hypoxic fetal

L-arginine prevents hypoxia-induced vasoconstriction in dual-perfused human placental cotyledons.

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BACKGROUND Chronic hypoxia in the uteroplacental unit is associated with increased resistance to blood flow in the fetal-placental circulation. These changes can lead to adverse cardiovascular events in adulthood. This study investigates whether L-arginine (substrate for nitric oxide synthase (NOS)

Hypoxia-induced fetoplacental vasoconstriction in perfused human placental cotyledons.

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Effects of maternal hypoxia on fetoplacental vascular resistance in the human placenta were investigated in an in vitro model in which single anatomic subunits (cotyledons) from term placentas were perfused at constant flow through both fetal and maternal circuits by means of a physiologic salt
OBJECTIVE The purpose of this study was to test the hypothesis that hypoxia down-regulates placental syncytin, which could play a role in altered placentogenesis; we investigated the influence of hypoxia on syncytin and its receptor ASCT2 gene expression in BeWo cells and in ex vivo perfused human

IFPA senior award lecture: Energy metabolism of human placental tissue studied by ex vivo perfusion of an isolated cotyledon.

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BACKGROUND This is a historical review of the method of "Ex vivo dual perfusion of a human placental cotyledon", which was first described by M. Panigel in 1967. The subsequent evolution of this method is described with particular emphasis on energy metabolism of human placental tissue under ex vivo
We hypothesized that placental resistance was elevated and transfer reduced in cotyledons from intrauterine growth-restricted (IUGR) fetuses. We perfused 10 cotyledons from term, normally grown fetuses, six from preterm, normally grown fetuses with normal umbilical arterial end-diastolic velocities
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