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Oxygen changes shift angiogenic factors to cause fetal growth restriction.

Women's Health Weekly

| October 02, 2003 | COPYRIGHT 2003 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2003 OCT 2 - (NewsRx.com & NewsRx.net) -- Oxygen changes shift angiogenic factors to cause fetal growth restriction.

"Placental growth factor (PlGF) and vascular endothelial growth factor (VEGF) are involved in placental angiogenesis through interactions with the VEGFR-1 and VEGFR-2 receptors. The placenta of pregnancies whose outcome is fetal growth restriction (FGR) are characterized by abnormal angiogenic development, classically associated with hypoxia. The present study evaluated the near-term expression of this growth factor family in an ovine model of placental insufficiency-FGR, in relationship to uteroplacental oxygenation," scientists in the United States reported.

"Compared to controls, FGR pregnancies demonstrated a 37 % increase in uterine blood flow (FGR vs. control, 610.86[+ or -]48.48 vs. 443.17[+ or -]37.39 ml min[superscript]-1 (kg fetus)[superscript]-1; p

"Maternal caruncle PlGF mRNA was increased in FGR (p

"The data establish that uterine blood flow is not reduced in relationship to metabolic demands in this FGR model and that the transplacental P-O[subscript]2 gradient is increased, maintaining umbilical oxygen uptake per unit of tissue. Furthermore, these data suggest that an increased transplacental gradient of oxygen generates changes in angiogenic growth factors, which may underline the pathophysiology of the post-placental hypoxic FGR," researchers concluded.

Regnault and colleagues published their study in Journal of Physiology - London (The relationship between transplacental O[subscript]2 diffusion and placental ...

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