Maternal binge drinking and fetal neuronal damage

@article{Wood2007MaternalBD,
  title={Maternal binge drinking and fetal neuronal damage},
  author={Charles E Wood},
  journal={Experimental Physiology},
  year={2007},
  volume={92}
}
  • C. Wood
  • Published 1 September 2007
  • Medicine
  • Experimental Physiology
Maternal binge drinking has obvious detrimental effects on the developing fetus. These effects include development of the phenotype of the fetal alcohol spectrum disorder and disordered development of the central nervous system (CNS). The mechanism of the CNS damage has been speculated to be fetal hypoxia or, perhaps more pertinently, fetal CNS tissue hypoxia. This hypothesis is not easily examined in small animal models of fetal alcohol exposure because of the inaccessibility of the developing… 
1 Citations

References

SHOWING 1-4 OF 4 REFERENCES
Binge alcohol exposure in the second trimester attenuates fetal cerebral blood flow response to hypoxia.
TLDR
Prenatal alcohol exposure during the second trimester attenuates cerebrovascular responses to hypoxia in the third trimester, which might set the stage for further brain injury if a hypoxic insult occurs.
Effect of age and blood pressure on the heart rate, vasopressin, and renin response to hypoxia in fetal sheep.
TLDR
It is concluded that increases in MAP and CVP do not influence the decrease in heart rate and lack of renin responses to acute hypoxia in the sheep fetus and that increased MAP andCVP seems to restrain the AVP response to hypoxIA in younger sheep fetuses.
Cardiovascular Responses to Hypoxemia in Sinoaortic-Denervated Fetal Sheep
TLDR
Intact fetuses showed an early hypertensive response to hypoxemia, whereas the sinoaortic-denervated fetuses developed a delayed, progressive rise in blood pressure, and fetal cardiac output and umbilical blood flow were maintained.
Chronic ethanol increases fetal cerebral blood flow specific to the ethanol‐sensitive cerebellum under normoxaemic, hypercapnic and acidaemic conditions: ovine model
TLDR
It is concluded that repeated exposure to moderate doses of ethanol during the third trimester alters fetal cerebral vascular function and increases blood flow in brain regions that are vulnerable to ethanol in the presence of acidaemia and hypercapnia, and in the absence of hypoxia.