Evidence map›Paper›PMID 20234380›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2010

Alterations in nitric oxide and endothelin-1 bioactivity underlie cerebrovascular dysfunction in ApoE-deficient mice.

Kazuo Yamashiro, Alexandra B Milsom, Johan Duchene, Catherine Panayiotou, Takao Urabe, Nobutaka Hattori, Amrita Ahluwalia

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  4. Review
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  10. Mouse models to study the effect of cardiovascular risk factors on brain structure and cognition.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013
    Review
  11. Hyperlipidemia disrupts cerebrovascular reflexes and worsens ischemic perfusion defect.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013
    Article
  12. The vascular endothelium in diabetes--a therapeutic target?Reviews in endocrine & metabolic disorders · 2013
    Review
  13. Genetics of cerebral vasospasm.Neurology research international · 2013
    Article
  14. Article
  15. Article
  16. Protecting against vascular disease in brain.American journal of physiology. Heart and circulatory physiology · 2011
    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

7 authors at 3 institutions in 2 countries.

Kazuo YamashiroClinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Charterhouse Square, London, UK.
Alexandra B Milsom
Johan Duchene
Catherine Panayiotou
Takao Urabe
Nobutaka Hattori
Amrita Ahluwalia
Queen Mary University of London · GBJuntendo University · JPWilliam Harvey Research Institute · GB

Funding

British Heart FoundationWellcome Trust
6 · The paper itself

Abstract

Hypercholesterolemia is associated with decreased nitric oxide (NO) bioavailability and endothelial dysfunction, a phenomenon thought to have a major role in the altered cerebral blood flow evident in stroke. Therefore, strategies that increase endothelial NO production have potential utility. Vascular reactivity of the middle cerebral artery (MCA) from C57BL/6J wild-type (WT) mice, apolipoprotein-E knockout (ApoE(-/-)) mice, and mice treated with the phosphodiesterase inhibitor cilostazol (100 mg/kg) was analyzed using the tension myograph. Contractile responses to endothelin-1 were significantly enhanced in MCA from ApoE(-/-) mice compared with WT mice (P<0.01), an effect absent in cilostazol-treated ApoE(-/-) mice. Acetylcholine-induced relaxation (which is entirely NO-dependent) was significantly impaired in MCA of ApoE(-/-) mice compared with WT mice (P<0.05), again an effect prevented by cilostazol treatment. Endothelial NOS phosphorylation at Ser(1179) was decreased in the aorta of ApoE(-/-) mice compared with WT mice (P<0.05), an effect normalized by cilostazol. Taken together, our data suggest that the endothelial dysfunction observed in MCA associated with hypercholesterolemia is prevented by cilostazol, an effect likely due to the increase in eNOS phosphorylation and, therefore, activity.

Indexed as

AnimalsAortaApolipoproteins ECells, CulturedCilostazolCyclic GMPEndothelin-1Endothelium, VascularHumansHypercholesterolemiaMaleMiceMice, Inbred C57BLMice, KnockoutMiddle Cerebral ArteryNitratesApolipoproteins ECilostazolCyclic GMPEndothelin-1NitratesNitric OxideNitric Oxide SynthaseNitritesPhosphodiesterase InhibitorsTetrazoles

Identifiers

PMID20234380
PMCPMC2949246
OpenAlexW2024723724

What OpenQuestion holds

Textmetadata
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.