Evidence map›Paper›PMID 22141380›Full record

ArticleAlcoholism, clinical and experimental research2012

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.

Shameena Bake, Joseph D Tingling, Rajesh C Miranda

Open access · greenAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
7.9field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Shameena BakeDepartment of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M Health Science Center, Bryan, USA.
Joseph D Tingling
Rajesh C Miranda
Texas A&M Health Science Center · US

Funding

Fetal Alcohol Exposure and NeurodevelopmentR01AA013440 · NIAAA · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI MIRANDA, RAJESH C · 2002 to 2012
$2.7M
NIAAA NIH HHS R01 AA013440NIAAA NIH HHS R01AA013440
6 · The paper itself

Abstract

backgroundEthanol (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.

methodsPregnant 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.

resultsBinge 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.

conclusionsThese 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.

Indexed as

Adaptation, PhysiologicalAlcohol DrinkingAnimalsCentral Nervous System DepressantsCerebrovascular CirculationEthanolFemaleFetal Alcohol Spectrum DisordersFetusHeadHemodynamicsInjections, IntraperitonealMaternal ExposureMicePregnancyPregnancy Trimester, SecondCentral Nervous System DepressantsEthanol

Identifiers

PMID22141380
PMCPMC3297711
OpenAlexW2136322496

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.