Prenatal Alcohol Exposure Reduces Placental Perfusion & Fetal Oxygenation
Studies have shown prenatal alcohol exposure increases the risk of preterm birth, stillbirth, decreased fetal growth, and fetal alcohol spectrum disorder (FASD). A recent experimental study added further value suggesting early chronic prenatal alcohol exposure significantly diminished placental perfusion at middle and late gestation and significantly decreased the oxygen supply to the...
Studies have shown prenatal alcohol exposure increases the risk of preterm birth, stillbirth, decreased fetal growth, and fetal alcohol spectrum disorder (FASD). A recent experimental study added further value suggesting early chronic prenatal alcohol exposure significantly diminished placental perfusion at middle and late gestation and significantly decreased the oxygen supply to the fetal vasculature throughout pregnancy in the rhesus macaque. The study findings were published in the American Journal of Obstetrics & Gynecology on January 01, 2022.
The placenta occupies a central role in supporting normal fetal growth and development during pregnancy. Previous studies suggest that prenatal alcohol exposure decreased both placental perfusion and fetal oxygen supply in midgestation and was associated with a decrease in both fetal and brain weight. However, the underlying mechanisms contributing to the observed altered placental function and fetal development were not explored. Therefore, Dr Jamie O. Lo and his team conducted an experimental study to determine the effect of early prenatal alcohol exposure on nonhuman primate placental function and fetal growth. They hypothesized that early chronic prenatal alcohol would alter placental perfusion and oxygen availability that adversely affects fetal growth.
In this study, the researchers included the subset of time-mated pregnant rhesus macaques (n=24) consisting of 12 control and 12 ethanol-exposed animals that underwent placental collection at the time of delivery. During the term, they assessed the radiographic images of all animals with Doppler ultrasound to measure fetal biometry, uterine artery volume blood flow, and placental volume blood flow. Following Doppler ultrasound, they assessed the findings of both:
♦ Blood oxygenation level-dependent magnetic resonance imaging to characterize placental blood oxygenation and
♦Dynamic contrast-enhanced magnetic resonance imaging to quantify maternal placental perfusion. Post-term, they performed the histologic and RNA-sequencing analyses on collected placental tissue.
Key findings of the study:
- Upon evaluation using Doppler, the researchers found that placental volume blood flow was decreased at all gestational time points in ethanol-exposed vs control animals, but most significantly at gestational day 110.
- They observed a significant decrease in total volumetric blood flow occurred in ethanol-exposed vs control animals on dynamic contrast-enhanced magnetic resonance imaging at both gestation days 110 and 135.
- Also, they noted a global reduction in T2∗, high blood deoxyhemoglobin concentration, occurred throughout gestation.
- Upon histologic analysis, they found a significant increase in microscopic infarctions in the ethanol-exposed group, largely present at middle to late gestation.
- Although fetal biometry and weight were decreased in ethanol-exposed vs control animals, they noted that the decrease was non-significant.
- Using RNA sequencing, they found the involvement of the inflammatory and extracellular matrix response pathways.
The authors concluded, "Early chronic prenatal alcohol exposure significantly diminished placental perfusion at mid to late gestation and also significantly decreased the oxygen supply to the fetal vasculature throughout pregnancy, these findings were associated with the presence of microscopic placental infarctions in the nonhuman primate."
They further added, "Although placental adaptations may compensate for early environmental perturbations to fetal growth, placental blood flow and oxygenation were reduced, consistent with the evidence of placental ischemic injury."
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