Evidence map›Paper›PMID 28554529›Full record

ArticleAlcohol (Fayetteville, N.Y.)2017

Maternal alcohol exposure during mid-pregnancy dilates fetal cerebral arteries via endocannabinoid receptors.

Olga Seleverstov, Ana Tobiasz, J Scott Jackson, Ryan Sullivan, Dejian Ma, J Pierce Sullivan, Steven Davison, Yada Akkhawattanangkul, Danielle L Tate, Terry Costello and 5 more

Abstract read
In one paragraph

Article in Alcohol (Fayetteville, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Review
  3. 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

15 authors at 1 institution in 1 country.

Olga SeleverstovDepartment of Pharmacology, University of Tennessee Health Science Center, Memphis, TN, USA.
Ana TobiaszDepartment of Obstetrics and Gynecology, University of Tennessee Health Science Center, Memphis, TN, USA.
J Scott JacksonDepartment of Comparative Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.
Ryan SullivanDepartment of Comparative Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.
Dejian MaDepartment of Pharmaceutical Sciences, College of Pharmacy, University of Tennessee Health Science Center, Memphis, TN, USA.
J Pierce SullivanDepartment of Comparative Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.
Steven DavisonDepartment of Comparative Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.
Yada AkkhawattanangkulDepartment of Comparative Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.
Danielle L TateDepartment of Obstetrics and Gynecology, University of Tennessee Health Science Center, Memphis, TN, USA.
Terry CostelloDepartment of Comparative Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.
Stacey BarnettDepartment of Comparative Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.
Wei LiDepartment of Pharmaceutical Sciences, College of Pharmacy, University of Tennessee Health Science Center, Memphis, TN, USA.
Giancarlo MariDepartment of Obstetrics and Gynecology, University of Tennessee Health Science Center, Memphis, TN, USA.
Alex M DopicoDepartment of Pharmacology, University of Tennessee Health Science Center, Memphis, TN, USA.
Anna N BukiyaDepartment of Pharmacology, University of Tennessee Health Science Center, Memphis, TN, USA. Electronic address: abukiya@uthsc.edu.
University of Tennessee Health Science Center · US

Funding

Baboon Research Resource ProgramP40OD010988 · OD · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI BANKS, RON E · 2012 to 2018
$9.0M
Fetal cerebrovascular eCB system as a target of maternal alcohol consumptionR21AA022433 · NIAAA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI BUKIYA, ANNA · 2014 to 2015
$387k
Mass Spectrometer for Small Molecule Drug DevelopmentS10OD016226 · OD · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MEIBOHM, BERND · 2014 to 2014
$316k
NIAAA NIH HHS R21 AA022433NIH HHS P40 OD010988NIH HHS S10 OD016226
6 · The paper itself

Abstract

Prenatal alcohol exposure often results in fetal alcohol syndrome and fetal alcohol spectrum disorders. Mechanisms of fetal brain damage by alcohol remain unclear. We used baboons (Papio spp.) to study alcohol-driven changes in the fetal cerebral artery endocannabinoid system. Pregnant baboons were subjected to binge alcohol exposure via gastric infusion three times during a period equivalent to the second trimester of human pregnancy. A control group was infused with orange-flavored drink that was isocaloric to the alcohol-containing solution. Cesarean sections were performed at a time equivalent to the end of the second trimester of human pregnancy. Fetal cerebral arteries were harvested and subjected to in vitro pressurization followed by pharmacological profiling. During each alcohol-infusion episode, maternal blood alcohol concentrations (BAC) reached 80 mg/dL, that is, equivalent to the BAC considered legal intoxication in humans. Circulating anandamide (AEA) and 2-arachidonoylglycerol (2-AG) remained unchanged. Ultrasound studies on pregnant mothers revealed that fetal alcohol exposure decreased peak systolic blood velocity in middle cerebral arteries when compared to pre-alcohol levels. Moreover, ethanol-induced dilation was observed in fetal cerebral arteries pressurized in vitro. This dilation was abolished by the mixture of AM251 and AM630, which block cannabinoid receptors 1 and 2, respectively. In the presence of AM251, the cannabinoid receptor agonist AEA evoked a higher, concentration-dependent dilation of cerebral arteries from alcohol-exposed fetuses. The difference in AEA-induced cerebral artery dilation vanished in the presence of AM630. CB1 and CB2 receptor mRNA and protein levels were similar in cerebral arteries from alcohol-exposed and control-exposed fetuses. In summary, alcohol exposure dilates fetal cerebral arteries via endocannabinoid receptors and results in an increased function of CB2.

Indexed as

Alcohol DrinkingAnimalsCerebral ArteriesCesarean SectionEndocannabinoidsEthanolFemaleFetal Alcohol Spectrum DisordersFetusGestational AgeHumansMaternal-Fetal ExchangePapioPregnancyReceptor, Cannabinoid, CB2Receptors, CannabinoidEndocannabinoidsEthanolReceptor, Cannabinoid, CB2Receptors, CannabinoidBaboon pregnancyBinge drinking during pregnancyFetal alcohol exposureFetal cerebral arteryMaternal alcohol consumption

Identifiers

PMID28554529
PMCPMC5517095
OpenAlexW2616293370

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.