Placental vascular development and neonatal outcome

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Abstract

The juxtaposition of the maternal and fetal circulations allows optimal physiological exchange between mother and fetus. Extravillous trophoblast infiltrating into the placental bed transforms the small calibre spiral arteries into large calibre uteroplacental arteries. The absence of these physiological changes, coupled with other lesions such as acute atherosis, results in a reduced uteroplacental blood flow, as seen in pre-eclampsia, intrauterine growth restriction and preterm delivery. A failure to elaborate the placental vascular tree can result in impaired flow through the fetal placental circulation. Placental vascular malformations, such as placental mesenchymal dysplasia and the commoner chorangioma, can lead to neonatal complications. Fetal thrombotic vasculopathy, commonly associated with thrombophilia, may be a cause of neurological deficit in childhood. © 2004 Elsevier Ltd. All rights reserved.

Author-supplied keywords

  • *placenta circulation
  • *placenta development
  • cell infiltration
  • clinical feature
  • dihydrofolate reductase/ec [Endogenous Compound]
  • dysplasia
  • fetus circulation
  • fibrin/ec [Endogenous Compound]
  • genetic polymorphism
  • human
  • intrauterine growth retardation
  • mother fetus relationship
  • neurologic disease/co [Complication]
  • newborn
  • placenta
  • placenta villus
  • preeclampsia
  • pregnancy
  • premature labor
  • review
  • thrombophilia/et [Etiology]
  • trophoblast
  • vascular disease
  • vascular lesion

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