Evidence map›Paper›PMID 25831209›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2015

Role of mitochondrial ATP-sensitive potassium channel-mediated PKC-ε in delayed protection against myocardial ischemia/reperfusion injury in isolated hearts of sevoflurane-preconditioned rats.

C Wang, S M Hu, H Xie, S G Qiao, H Liu, C F Liu

Open access · goldAbstract readEvaluation Study
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
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  10. Purinergic Signalling: Therapeutic Developments.Frontiers in pharmacology · 2017
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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.

C WangDepartment of Anesthesiology and Critical Care, The Second Affiliate Hospital, Soochow University, Suzhou, China.
S M HuInstitute of Neuroscience, Soochow University, Suzhou, China.
H XieDepartment of Anesthesiology and Critical Care, The Second Affiliate Hospital, Soochow University, Suzhou, China.
S G QiaoDepartment of Anesthesiology and Critical Care, The Second Affiliate Hospital, Soochow University, Suzhou, China.
H LiuDepartment of Anesthesiology and Pain Medicine, University of California Davis Health System, Davis, CA, USA.
C F LiuInstitute of Neuroscience, Soochow University, Suzhou, China.
Soochow University · CNUC Davis Health System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to determine the role of mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channels and protein kinase C (PKC)-ε in the delayed protective effects of sevoflurane preconditioning using Langendorff isolated heart perfusion models. Fifty-four isolated perfused rat hearts were randomly divided into 6 groups (n=9). The rats were exposed for 60 min to 2.5% sevoflurane (the second window of protection group, SWOP group) or 33% oxygen inhalation (I/R group) 24 h before coronary occlusion. The control group (CON) and the sevoflurane group (SEVO) group were exposed to 33% oxygen and 2.5% sevoflurane for 60 min, respectively, without coronary occlusion. The mitoKATP channel inhibitor 5-hydroxydecanoate (5-HD) was given 30 min before sevoflurane preconditioning (5-HD+SWOP group). Cardiac function indices, infarct sizes, serum cardiac troponin I (cTnI) concentrations, and the expression levels of phosphorylated PKC-ε (p-PKC-ε) and caspase-8 were measured. Cardiac function was unchanged, p-PKC-ε expression was upregulated, caspase-8 expression was downregulated, cTnI concentrations were decreased, and the infarcts were significantly smaller (P<0.05) in the SWOP group compared with the I/R group. Cardiac function was worse, p-PKC-ε expression was downregulated, caspase-8 expression was upregulated, cTnI concentration was increased and infarcts were larger in the 5-HD+SWOP group (P<0.05) compared with the SWOP group. The results suggest that mitoKATP channels are involved in the myocardial protective effects of sevoflurane in preconditioning against I/R injury, by regulating PKC-ε phosphorylation before ischemia, and by downregulating caspase-8 during reperfusion.

Indexed as

AnimalsAnti-Arrhythmia AgentsBlotting, WesternCaspase 8Decanoic AcidsHeartHemodynamicsHydroxy AcidsIschemiaIschemic Preconditioning, MyocardialMaleMethyl EthersMyocardial Reperfusion InjuryPlatelet Aggregation InhibitorsPotassium ChannelsProtective Agents5-hydroxydecanoic acidAnti-Arrhythmia AgentsCaspase 8Decanoic AcidsHydroxy AcidsMethyl Ethersmitochondrial K(ATP) channelPlatelet Aggregation InhibitorsPotassium ChannelsProtective AgentsProtein Kinase CSevofluraneTroponin I

Identifiers

PMID25831209
PMCPMC4470312
OpenAlexW2038407666

What OpenQuestion holds

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LicenceCC BY-NC
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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.