Evidence map›Paper›PMID 24154701›Full record

ArticleBritish journal of anaesthesia2014

Activation of K(2)P channel-TREK1 mediates the neuroprotection induced by sevoflurane preconditioning.

L Tong, M Cai, Y Huang, H Zhang, B Su, Z Li, H Dong

Open access · bronzeAbstract read
In one paragraph

Article in British journal of anaesthesia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. ATF5-Dependent GDF15 Expression Mediates Anesthesia-Induced Neuroprotection Against Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  7. Review
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  12. Review
  13. Review
  14. [Carbon Monoxide and Pain Regulation: A Review].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021
    Review
  15. Article
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  17. Article
  18. Review
  19. 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

7 authors at 1 institution in 1 country.

L TongDepartment of Anesthesiology, Xijing Hospital, Xi'an, Shanxi 710032, China.
M CaiDepartment of Anesthesiology, Xijing Hospital, Xi'an, Shanxi 710032, China.
Y HuangDepartment of Anesthesiology, Xijing Hospital, Xi'an, Shanxi 710032, China.
H ZhangDepartment of Anesthesiology, Xijing Hospital, Xi'an, Shanxi 710032, China.
B SuDepartment of Anesthesiology, Xijing Hospital, Xi'an, Shanxi 710032, China.
Z LiDepartment of Anesthesiology, Xijing Hospital, Xi'an, Shanxi 710032, China.
H DongDepartment of Anesthesiology, Xijing Hospital, Xi'an, Shanxi 710032, China hldong6@hotmail.com.
Xijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPreconditioning with volatile anaesthetic agents induces tolerance to focal cerebral ischaemia, although the underlying mechanisms have not been clearly defined. The present study analyses whether TREK-1, a two-pore domain K(+) channel and target for volatile anaesthetics, plays a role in mediating neuroprotection by sevoflurane.

methodsDifferentiated SH-SY5Y cells were preconditioning with sevoflurane and challenged by oxygen-glucose deprivation (OGD). Cell viability and expression of caspase-3 and TREK-1 were evaluated. Rats that were preconditioned with sevoflurane were subjected to middle cerebral artery occlusion (MCAO), and the expression of TREK-1 protein and mRNA was analysed. Neurological scores were evaluated and infarction volume was examined.

resultsSevoflurane preconditioning reduced cell death in differentiated SH-SY5Y cells challenged by OGD. Sevoflurane preconditioning reduced infarct volume and improved neurological outcome in rats subjected to MCAO. Sevoflurane preconditioning increased levels of TREK-1 mRNA and protein. Knockdown of TREK-1 significantly attenuated sevoflurane preconditioning-induced neuroprotective effects in vitro and in vivo.

conclusionsSevoflurane preconditioning-induced neuroprotective effects against transient cerebral ischaemic injuries involve TREK-1 channels. These results suggest a novel mechanism for sevoflurane preconditioning-induced tolerance to focal cerebral ischaemia.

Indexed as

AnimalsBrainBrain IschemiaCarbon MonoxideCell DifferentiationCell HypoxiaCell SurvivalCerebral InfarctionGene Knockdown TechniquesHumansIschemic PreconditioningMaleMethyl EthersNeuroprotective AgentsOxygenPartial PressureCarbon MonoxideMethyl EthersNeuroprotective AgentsOxygenpotassium channel protein TREK-1Potassium Channels, Tandem Pore DomainRNA, MessengerRNA, Small InterferingSevofluraneanaesthetics volatile, sevofluranebrain, ischaemianeuroprotectionpreconditioningTREK-1

Identifiers

PMID24154701
PMCPMC4062297
OpenAlexW2103287160

What OpenQuestion holds

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LicenceCC BY-NC
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.