Document Detail


Ethanol exposure during pregnancy persistently attenuates cranially directed blood flow in the developing fetus: evidence from ultrasound imaging in a murine second trimester equivalent model.
MedLine Citation:
PMID:  22141380     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Ethanol (EtOH) consumption during pregnancy can lead to fetal growth retardation, mental retardation, and neurodevelopmental delay. The fetal brain initiates neurogenesis and vasculogenesis during the second trimester, and depends on maternal-fetal circulation for nutrition and growth signals. We used high-resolution in vivo ultrasound imaging to test the hypothesis that EtOH interferes with fetal brain-directed blood flow during this critical developmental period.
METHODS: Pregnant mice were lightly anesthetized on gestational day 12 with an isoflurane/oxygen mixture. We assessed the effect of single and repeated binge-like maternal EtOH exposures at 3 g/kg, administered by intragastric gavage or intraperitoneal injection, on maternal circulation and fetal umbilical, aortic, internal carotid, and middle cerebral arterial circulation.
RESULTS: Binge maternal EtOH exposure, regardless of exposure route, significantly reduced fetal arterial blood acceleration and velocity time integral (VTI), from umbilical to cerebral arteries, without a change in fetal heart rate and resistivity indices. Importantly a single maternal binge EtOH exposure induced persistent suppression of fetal arterial VTI for at least 24 hours. Repeated binge episodes resulted in a continuing and persistent suppression of fetal VTI. Qualitative assessments showed that maternal EtOH exposure induced oscillatory, nondirectional blood flow in fetal cerebral arteries. Maternal cardiac and other physiological parameters remained unaltered.
CONCLUSIONS: These data show that binge-type maternal EtOH exposure results in rapid and persistent loss of blood flow from the umbilical artery to the fetal brain, potentially compromising nutrition and the maternal/fetal endocrine environment during a critical period for neuron formation and angiogenesis in the maturing brain.
Authors:
Shameena Bake; Joseph D Tingling; Rajesh C Miranda
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-12-05
Journal Detail:
Title:  Alcoholism, clinical and experimental research     Volume:  36     ISSN:  1530-0277     ISO Abbreviation:  Alcohol. Clin. Exp. Res.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-05-02     Completed Date:  2012-09-10     Revised Date:  2014-09-09    
Medline Journal Info:
Nlm Unique ID:  7707242     Medline TA:  Alcohol Clin Exp Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  748-58     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 by the Research Society on Alcoholism.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological
Alcohol Drinking / adverse effects
Animals
Central Nervous System Depressants / administration & dosage,  adverse effects*,  blood
Cerebrovascular Circulation / drug effects*
Ethanol / administration & dosage,  adverse effects*,  blood
Female
Fetal Alcohol Spectrum Disorders / etiology*
Fetus / blood supply,  drug effects*
Head / blood supply
Hemodynamics / drug effects
Injections, Intraperitoneal
Maternal Exposure / adverse effects
Mice
Pregnancy
Pregnancy Trimester, Second
Respiration / drug effects
Ultrasonography, Prenatal
Grant Support
ID/Acronym/Agency:
R01 AA013440/AA/NIAAA NIH HHS; R01 AA013440-06A1S1/AA/NIAAA NIH HHS; R01 AA013440-09/AA/NIAAA NIH HHS; R01 AA013440-10/AA/NIAAA NIH HHS; R01AA013440/AA/NIAAA NIH HHS
Chemical
Reg. No./Substance:
0/Central Nervous System Depressants; 3K9958V90M/Ethanol
Comments/Corrections

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