Evidence map›Paper›PMID 30748017›Full record

ArticleAlcoholism, clinical and experimental research2019

In Utero Exposure to Alcohol Impairs Reactivity of Cerebral Arterioles and Increases Susceptibility of the Brain to Damage Following Ischemia/Reperfusion in Adulthood.

Sergio G Cananzi, William G Mayhan

Open access · greenAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. In utero hypoxia attenuated acetylcholine-mediated vasodilatation via CHRM3/p-NOS3 in fetal sheep MCA: role of ROS/ERK1/2.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Article
  10. Review
  11. Article
  12. Article
  13. Fetal Cerebral Artery Mitochondrion as Target of Prenatal Alcohol Exposure.International journal of environmental research and public health · 2019
    Review
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

2 authors at 2 institutions in 1 country.

Sergio G CananziDepartment of Molecular Biology , University of Texas-Southwestern, Dallas, Texas.
William G MayhanDivision of Basic Biomedical Sciences , Sanford School of Medicine, University of South Dakota, Vermillion, South Dakota.ORCID 0000-0003-2810-0137
The University of Texas Southwestern Medical Center · USUniversity of South Dakota · US

Funding

Dysfunction of the Cerebral Microcirculation by In Utero Exposure to AlcoholR01AA027206 · NIAAA · UNIVERSITY OF SOUTH DAKOTA · PI MAYHAN, WILLIAM G · 2018 to 2021
$1.3M
Malcolm Feist Fellowship from LSU Health Sciences Center-ShreveportNIAAA NIH HHS R01 AA027206Sanford School of Medicine at the University of South Dakota
6 · The paper itself

Abstract

backgroundMaternal consumption of alcohol produces abnormalities in the developing fetus and can contribute to an increased incidence of many cardiovascular-related diseases. The first goal of this study was to determine whether in utero exposure to alcohol influences reactivity of cerebral arterioles in adult (12 to 15 weeks old) rats. The second goal of this study was to examine whether in utero exposure to alcohol increased the susceptibility of the brain to damage following an ischemic event in adult rats.

methodsWe fed Sprague Dawley dams a liquid diet with or without alcohol (3% ethanol) for the duration of their pregnancy (21 to 23 days). In the first series of studies, we examined reactivity of cerebral arterioles to endothelial nitric oxide synthase (eNOS)- (adenosine diphosphate [ADP]) and neuronal nitric oxide synthase (nNOS)-dependent N-methyl-D-aspartate (NMDA, and NOS-independent agonists in adult rats before and during application of l-NMMA. In another series of studies, we examined infarct volume following middle cerebral artery occlusion in adult offspring exposed to alcohol in utero. In both series of studies, we also determined the role for an increase in oxidative stress by feeding dams apocynin for the duration of their pregnancy.

resultsWe found that in utero exposure to alcohol reduced responses of cerebral arterioles to ADP and NMDA, but not to nitroglycerin in adult rats. In addition, treatment of the dams with apocynin prevented this impairment in cerebral vascular function. We also found that in utero exposure to alcohol worsened brain damage following ischemia/reperfusion in adult rats and that treatment of dams with apocynin prevented this increase in brain damage following ischemia/reperfusion.

conclusionsWe suggest that our findings may have important implications for the pathogenesis of brain abnormalities associated with fetal alcohol exposure.

Indexed as

AcetophenonesAdenosine DiphosphateAnimalsArteriolesBrainEnzyme InhibitorsEthanolExcitatory Amino Acid AgonistsFemaleInfarctionInfarction, Middle Cerebral ArteryMaleNitroglycerinN-Methylaspartateomega-N-MethylargininePregnancyAcetophenonesacetovanilloneAdenosine DiphosphateEnzyme InhibitorsEthanolExcitatory Amino Acid AgonistsNitroglycerinN-Methylaspartateomega-N-MethylarginineCerebral Vascular FunctionFetal Alcohol SyndromeNitric OxideOxidative StressStroke

Identifiers

PMID30748017
PMCPMC6538292
OpenAlexW2911284866

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.