Evidence map›Paper›PMID 24962648›Full record

ArticleAlcoholism, clinical and experimental research2014

Chronic binge alcohol exposure during pregnancy impairs rat maternal uterine vascular function.

Kaviarasan Subramanian, Vishal D Naik, Kunju Sathishkumar, Chandrashekar Yallampalli, George R Saade, Gary D Hankins, Jayanth Ramadoss

Open access · greenAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

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  18. Fetal regional brain protein signature in FASD rat model.Reproductive toxicology (Elmsford, N.Y.) · 2018
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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

7 authors at 1 institution in 1 country.

Kaviarasan SubramanianDepartment of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, Texas.
Vishal D Naik
Kunju Sathishkumar
Chandrashekar Yallampalli
George R Saade
Gary D Hankins
Jayanth Ramadoss
The University of Texas Medical Branch at Galveston · US

Funding

Maternal Uterine Vascular Origins of Fetal Alcohol Spectrum DisordersR00AA019446 · NIAAA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI RAMADOSS, JAYANTH · 2011 to 2013
$730k
Maternal Uterine Vascular Origins of Fetal Alcohol Spectrum DisordersK99AA019446 · NIAAA · UNIVERSITY OF WISCONSIN-MADISON · PI RAMADOSS, JAYANTH · 2010 to 2011
$267k
NIAAA NIH HHS AA19446NIAAA NIH HHS K99 AA019446NIAAA NIH HHS R00 AA019446
6 · The paper itself

Abstract

backgroundAlcohol exposure during pregnancy results in an array of structural and functional abnormalities called fetal alcohol spectrum disorders (FASD). Alcohol dysregulates the exquisite coordination and regulation of gestational adaptations at the level of the uterine vasculature. We herein hypothesized that chronic binge-like alcohol results in uterine vascular dysfunction and impairs maternal uterine artery reactivity to vasoconstrictors and dilators.

methodsWe utilized a once-daily binge alcohol (4.5 g/kg body weight) exposure paradigm (gestational day 7 to 17) in a pregnant rat model system and investigated primary uterine artery function in response to vasoconstrictors and vasodilators utilizing wire myography.

resultsAlcohol (peak blood alcohol concentration, 216 mg/dl) produced uterine vascular dysfunction. Alcohol did not produce altered uterine vascular reactivity to α1 adrenergic agonist phenylephrine or the prostanoid thromboxane. However, alcohol specifically impaired acetylcholine (ACh)-mediated uterine artery vasodilation but exogenous endothelium-independent vasodilators like sodium nitroprusside exhibited no alcohol effect; ACh significantly decreased vessel relaxation (p = 0.003; ↓pD2 [negative log molar ACh concentration producing the half maximum response], -7.004 ± 0.215 vs. -6.310 ± 0.208; EMax [maximal ACh response], 92% vs. 75%).

conclusionsWe conclude that moderate alcohol exposure impairs uterine vascular function in pregnant mothers. Alcohol specifically impairs agonist-induced uterine artery vasodilation. In summary, the maternal uterine compartment may play a significant role in the pathogenesis of FASD. Thus, the mechanistic targets of alcohol at the level of both the mother and the fetus need to be considered in order to develop effective therapeutic treatment strategies for FASD.

Indexed as

AcetylcholineAnimalsBinge DrinkingDose-Response Relationship, DrugEthanolFemaleNitroprussidePhenylephrinePlacental CirculationPregnancyRatsThromboxanesUterine ArteryVasoconstrictionVasoconstrictor AgentsVasodilationAcetylcholineEthanolNitroprussidePhenylephrineThromboxanesVasoconstrictor AgentsVasodilator AgentsAlcoholEndotheliumFetal Alcohol Spectrum DisordersMaternalUterineVascular

Identifiers

PMID24962648
PMCPMC4107157
OpenAlexW2148424419

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.