Evidence map›Paper›PMID 31576483›Full record

ArticleNeurocritical care2020

Cyclosporine A Plus Ischemic Postconditioning Improves Neurological Function in Rats After Cardiac Resuscitation.

Xiang Zhou, YanLiang Qu, GuoShen Gan, ShuiBo Zhu, Yang Huang, Yong Liu, Jian Zhu, Biao Xie, ZhiTian Tan

Abstract read
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In one paragraph

Article in Neurocritical care, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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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

9 authors at 5 institutions in 1 country.

Xiang Zhou *Department of Anesthesiology, General Hospital of Central Theater Command of People's Liberation Army of China, Wuhan, China.
YanLiang Qu *Department of Anesthesiology, No. 971 Hospital of the PLA Navy, Qingdao, China.
GuoShen GanSouthern Medical University, Guangzhou, China.
ShuiBo ZhuDepartment of Thoracic Cardiovascular Surgery, General Hospital of Central Theater Command of People's Liberation Army of China, 627 Wuluo Road, Wuhan, 430070, Hubei, China. whzyyzsb@126.com.ORCID http://orcid.org/0000-0003-2069-7338
Yang HuangSouthern Medical University, Guangzhou, China.
Yong LiuDepartment of Thoracic Cardiovascular Surgery, General Hospital of Central Theater Command of People's Liberation Army of China, 627 Wuluo Road, Wuhan, 430070, Hubei, China.
Jian ZhuDepartment of Thoracic Cardiovascular Surgery, General Hospital of Central Theater Command of People's Liberation Army of China, 627 Wuluo Road, Wuhan, 430070, Hubei, China.
Biao XieSouthern Medical University, Guangzhou, China.
ZhiTian TanSouthern Medical University, Guangzhou, China.
Southern Medical University · CNGeneral Hospital of Central Theater CommandCentral Hospital of Wuhan · CNPeople's Liberation Army 401 Hospital · CNWuhan General Hospital of Guangzhou · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectiveAttenuation of neuronal apoptosis helps maintain neurological function in patients after cardiac arrest. After ischemia-reperfusion, both cyclosporin A (CsA) and ischemic postconditioning independently protect mitochondria and thus reduce nerve injury. This study employed a rat model to evaluate the neuroprotective effect of combining ischemic postconditioning with CsA after cardiopulmonary resuscitation (CPR).

methodsRats were apportioned equally to model control, postconditioned, CsA-treated, or CsA + postconditioned groups. Asphyxial cardiac arrest was imposed using modified Utstein-style guidelines. In the appropriate groups, postconditioning was implemented by ischemia and reperfusion (clamping and loosening the left femoral artery); CsA treatment was delivered with a single intravenous dose. Neurological deficits were scored at different times after CPR. Histological evaluation and electron microscopy were used to evaluate tissue damage, and TUNEL and flow cytometry were used to measure the apoptotic rate of hippocampal neurons and size of the mitochondrial permeability transition pore (mPTP) opening.

resultsThe apoptotic rate was significantly lower in the postconditioned and CsA-treated groups compared with the model control and lowest in the CsA + postconditioned group. By histological evaluation and electron microscopy, the least damage was observed in the CsA + postconditioned group. The neurological deficit score of the CsA + postconditioned group was significantly higher than that of the CsA-treated group, but the size of the mPTP openings of these two groups was comparable.

conclusionIschemic postconditioning combined with CsA exerted a better neuroprotective effect after CPR than did either postconditioning or CsA alone. Inhibiting the opening of the mPTP is not the only neuroprotective mechanism.

Indexed as

AnimalsApoptosisBrainCardiopulmonary ResuscitationCyclosporineEnzyme InhibitorsHeart ArrestIschemic PostconditioningMitochondrial Permeability Transition PoreNeuronsPost-Cardiac Arrest SyndromeRatsReperfusion InjuryCyclosporineEnzyme InhibitorsMitochondrial Permeability Transition PoreCardiopulmonary resuscitationCyclosporin AIschemic postconditioningMitochondrial permeability transition poreNeurological function

Identifiers

PMID31576483
OpenAlexW2978207279

What OpenQuestion holds

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Registered trials

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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.