Evidence map›Paper›PMID 36446735›Full record

ArticleAlcohol, clinical & experimental research2023

Prenatal exposure to alcohol impairs responses of cerebral arterioles to activation of potassium channels: Role of oxidative stress.

Partha S Saha, Tiffany M Knecht, Denise M Arrick, Michael J Watt, Jamie L Scholl, William G Mayhan

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Alcohol, clinical & experimental research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.7field-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

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. Alcohol Metabolism into Acetaldehyde in Developing Cerebral Arteries.International journal of molecular sciences · 2026
    Article
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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

6 authors at 2 institutions in 2 countries.

Partha S SahaDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, South Dakota, USA.
Tiffany M KnechtDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, South Dakota, USA.
Denise M ArrickDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, South Dakota, USA.
Michael J WattDepartment of Anatomy, University of Otago, Dunedin, New Zealand.
Jamie L SchollDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, South Dakota, USA.
William G MayhanDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, South Dakota, USA.ORCID 0000-0003-2810-0137
University of South Dakota · USUniversity of Otago · NZ

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
NIAAA NIH HHS R01 AA027206
6 · The paper itself

Abstract

backgroundPotassium channels play an important role in the basal tone and dilation of cerebral resistance arterioles in response to many stimuli. However, the effect of prenatal alcohol exposure (PAE) on specific potassium channel function remains unknown. The first goal of this study was to determine the influence of PAE on the reactivity of cerebral arterioles to activation of ATP-sensitive potassium (K

methodsWe fed Sprague-Dawley dams a liquid diet with or without alcohol (3% EtOH) for the duration of their pregnancy (21 to 23 days). We examined in vivo responses of cerebral arterioles in control and PAE male and female offspring (14 to 16 weeks after birth) to activators of potassium channels (Iloprost [BK channels] and pinacidil [K

resultsWe found that PAE impaired dilation of cerebral arterioles in response to activation of potassium channels with iloprost and pinacidil, and this impairment was similar in male and female rats. In addition, treatment with apocynin reversed the impaired vasodilation to iloprost and pinacidil in PAE rats to levels observed in control rats. This effect of apocynin also was similar in male and female rats.

conclusionsPAE induces dysfunction in the ability of specific potassium channels to dilate cerebral arterioles which appears to be mediated by an increase in oxidative stress. We suggest that these alterations in potassium channel function may contribute to the pathogenesis of cerebral vascular abnormalities and/or behavioral/cognitive deficits observed in fetal alcohol spectrum disorders.

Indexed as

Prenatal Exposure Delayed EffectsAcetophenonesAdenosine TriphosphateAnimalsArteriolesEthanolFemaleHumansIloprostLarge-Conductance Calcium-Activated Potassium ChannelsMaleOxidative StressPinacidilPregnancyRatsRats, Sprague-DawleyAcetophenonesacetovanilloneAdenosine TriphosphateEthanolIloprostLarge-Conductance Calcium-Activated Potassium ChannelsPinacidilVasodilator Agentsbraincerebral blood flowiloprost and pinacidilpial arteriolespotassium channels

Identifiers

PMID36446735
PMCPMC9974881
OpenAlexW4309717473

What OpenQuestion holds

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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.