Evidence map›Paper›PMID 25400168›Full record

ArticleScientific reports2014

Ventricular hypertrophy blocked delayed anesthetic cardioprotection in rats by alteration of iNOS/COX-2 signaling.

Leilei Ma, Feijuan Kong, Hongwei Ge, Jingquan Liu, Fangxiao Gong, Liang Xu, Bangchuan Hu, Renhua Sun

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

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. 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

8 authors at 3 institutions in 1 country.

Leilei Ma1] Department of Critical Care Medicine, Zhejiang Provincial People's Hospital, Hangzhou, China [2] Department of Anesthesiology, Hangzhou First People's Hospital, Nanjing Medical University, Hangzhou, China [3] Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Feijuan Kong1] Department of Anesthesiology, Hangzhou First People's Hospital, Nanjing Medical University, Hangzhou, China [2] Department of Endocrinology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Hongwei GeDepartment of Urology, Peking University Shougang Hospital, Beijing, China.
Jingquan LiuDepartment of Critical Care Medicine, Zhejiang Provincial People's Hospital, Hangzhou, China.
Fangxiao GongDepartment of Critical Care Medicine, Zhejiang Provincial People's Hospital, Hangzhou, China.
Liang XuDepartment of Critical Care Medicine, Zhejiang Provincial People's Hospital, Hangzhou, China.
Bangchuan HuDepartment of Critical Care Medicine, Zhejiang Provincial People's Hospital, Hangzhou, China.
Renhua SunDepartment of Critical Care Medicine, Zhejiang Provincial People's Hospital, Hangzhou, China.
Zhejiang Provincial People's Hospital · CNHangzhou First People's Hospital · CNPeking University Shougang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the current study was to determine whether ventricular hypertrophy affects the delayed isoflurane preconditioning against myocardial ischemia-reperfusion (IR) injury. Transverse aortic constriction (TAC) was performed on male Sprague-Dawley rats to induce left ventricular (LV) hypertrophy, then sham-operated or hypertrophied rat hearts were subjected to isoflurane preconditioning (2.1% v/v, 1 h). 24 h after exposure, the hearts were isolated and perfused retrogradely by the Langendorff for 30 min (equilibration) followed by 40 min of ischemia and then 120 min of reperfusion. The hemodynamics, infarct size, apoptosis, nitric oxide synthase (NOS), cyclooxygenase-2 (COX-2), Cleaved Caspase-3 and production of NO were determined. We found that the hemodynamic parameters were all markedly improved during the reperfusion period and the myocardial infarct size and apoptosis was significantly reduced by delayed isoflurane preconditioning in sham-operated rats. However, such cardiac improvement induced by delayed isoflurane preconditioning was not observed in hypertrophied hearts. The expression of iNOS, COX-2 and NO was markedly enhanced, whereas Cleaved Caspase-3 activity was inhibited by delayed isoflurane preconditioning in sham-operated rats, a phenomenon was not found in TAC-control groups pretreated with isoflurane. Our results demonstrated that ventricular hypertrophy abrogated isoflurane-induced delayed cardioprotection by alteration of iNOS/COX-2 pathway.

Indexed as

AnimalsApoptosisCaspase 3Cyclooxygenase 2HemodynamicsHumansHypertrophy, Left VentricularIsofluraneMaleMyocardial InfarctionMyocardial Reperfusion InjuryNitric OxideNitric Oxide Synthase Type IIRatsSignal TransductionCaspase 3Cyclooxygenase 2IsofluraneNitric OxideNitric Oxide Synthase Type IINos2 protein, ratPtgs2 protein, rat

Identifiers

PMID25400168
PMCPMC4233333
OpenAlexW2027417277

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.