Evidence map›Paper›PMID 24696844›Full record

ArticleBioMed research international2014

Impaired cerebral mitochondrial oxidative phosphorylation function in a rat model of ventricular fibrillation and cardiopulmonary resuscitation.

Jun Jiang, Xiangshao Fang, Yue Fu, Wen Xu, Longyuan Jiang, Zitong Huang

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

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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 1 institution in 1 country.

Jun JiangDepartment of Emergency Medicine, The First People's Hospital of Foshan, 81 Ling Nan Road, Foshan, Guangdong 528000, China ; Institute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, 107 Yan Jiang Xi Road, Guangzhou, Guangdong 510120, China.ORCID 0000-0002-1521-5421
Xiangshao FangInstitute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, 107 Yan Jiang Xi Road, Guangzhou, Guangdong 510120, China ; Department of Emergency Medicine, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, 107 Yan Jiang Xi Road, Guangzhou, Guangdong 510120, China.ORCID 0000-0002-9600-4115
Yue FuDepartment of Emergency Medicine, The First People's Hospital of Foshan, 81 Ling Nan Road, Foshan, Guangdong 528000, China ; Institute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, 107 Yan Jiang Xi Road, Guangzhou, Guangdong 510120, China.
Wen XuInstitute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, 107 Yan Jiang Xi Road, Guangzhou, Guangdong 510120, China ; Department of Emergency Medicine, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, 107 Yan Jiang Xi Road, Guangzhou, Guangdong 510120, China.
Longyuan JiangInstitute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, 107 Yan Jiang Xi Road, Guangzhou, Guangdong 510120, China ; Department of Emergency Medicine, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, 107 Yan Jiang Xi Road, Guangzhou, Guangdong 510120, China.
Zitong HuangInstitute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, 107 Yan Jiang Xi Road, Guangzhou, Guangdong 510120, China ; Department of Emergency Medicine, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, 107 Yan Jiang Xi Road, Guangzhou, Guangdong 510120, China.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Postcardiac arrest brain injury significantly contributes to mortality and morbidity in patients suffering from cardiac arrest (CA). Evidence that shows that mitochondrial dysfunction appears to be a key factor in tissue damage after ischemia/reperfusion is accumulating. However, limited data are available regarding the cerebral mitochondrial dysfunction during CA and cardiopulmonary resuscitation (CPR) and its relationship to the alterations of high-energy phosphate. Here, we sought to identify alterations of mitochondrial morphology and oxidative phosphorylation function as well as high-energy phosphates during CA and CPR in a rat model of ventricular fibrillation (VF). We found that impairment of mitochondrial respiration and partial depletion of adenosine triphosphate (ATP) and phosphocreatine (PCr) developed in the cerebral cortex and hippocampus following a prolonged cardiac arrest. Optimal CPR might ameliorate the deranged phosphorus metabolism and preserve mitochondrial function. No obvious ultrastructural abnormalities of mitochondria have been found during CA. We conclude that CA causes cerebral mitochondrial dysfunction along with decay of high-energy phosphates, which would be mitigated with CPR. This study may broaden our understanding of the pathogenic processes underlying global cerebral ischemic injury and provide a potential therapeutic strategy that aimed at preserving cerebral mitochondrial function during CA.

Indexed as

Cardiopulmonary ResuscitationOxidative PhosphorylationAnimalsBrainCell RespirationDisease Models, AnimalEnergy MetabolismHemodynamicsHippocampusMaleMitochondriaRats, Sprague-DawleyVentricular Fibrillation

Identifiers

PMID24696844
PMCPMC3947758
OpenAlexW2016346542

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.