Development and Mechanisms of Fetal Hypoxia in Severe Fetal Growth Restriction

Abstract Severe fetal growth restriction (FGR) is often associated with hypoxia. We studied FGR hypoxia in an experimental model which is produced by exposing pregnant ewes to a hyperthermic environment. The study utilized simultaneous measurements of several relevant factors, e.g., uterine and umbi...

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Bibliographic Details
Published in:Placenta (Eastbourne) 2007-07, Vol.28 (7), p.714-723
Main Authors: Regnault, T.R.H, de Vrijer, B, Galan, H.L, Wilkening, R.B, Battaglia, F.C, Meschia, G
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Blood Glucose
Body Temperature
Disease Models, Animal
Embryology: invertebrates and vertebrates. Teratology
Female
Fetal Blood - chemistry
Fetal Growth Retardation - etiology
Fetal Hypoxia - etiology
Fetus
Fundamental and applied biological sciences. Psychology
Heating
Insulin - blood
Internal Medicine
IUGR
Lactic Acid - blood
Maternal-Fetal Exchange
Obstetrics and Gynecology
Organ Size
Oxygen
Oxygen - blood
Oxygen - metabolism
Partial Pressure
Placenta
Placental Circulation
Pregnancy
Respiration
Sheep
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Summary:Abstract Severe fetal growth restriction (FGR) is often associated with hypoxia. We studied FGR hypoxia in an experimental model which is produced by exposing pregnant ewes to a hyperthermic environment. The study utilized simultaneous measurements of several relevant factors, e.g., uterine and umbilical blood flows and O2 uptakes. Sixteen ewes were divided equally into control (C) and hyperthermic (HT) groups. Hyperthermia (40 °C for 12 h/35 °C for 12 h; ∼35% relative humidity, RH) was maintained for 80 days commencing at approximately 38 days gestational age (dGA term 147 ± 3 days). All ewes were then placed in a control environment (∼21 °C, 24 h; ∼30% RH) and studied at approximately 134 dGA. Mean HT placental and fetal weights were 39% and 45% of C, respectively ( p < 0.0001), umbilical O2 uptake/kg fetus was 76% of C ( p < 0.01) and umbilical venous PO2 was reduced (20.2 vs. 29.7 Torr, p < 0.001). Contrary to the hypothesis that FGR hypoxia is due to maternal placental hypoperfusion, uterine flow was not reduced in relation to O2 uptake. The uterine–umbilical venous PO2 difference was enlarged (38 vs. 23 Torr, p < 0.0001). This difference is the expression of a balance between developmental changes in placental structure and oxidative metabolism, which have opposite effects in terms of fetal oxygenation. We postulate that FGR hypoxia results from disproportionate underdevelopment of those changes which allow for a progressive increase in umbilical O2 uptake.
ISSN:0143-4004
1532-3102
DOI:10.1016/j.placenta.2006.06.007