Evidence map›Paper›PMID 26010685›Full record

ArticleCritical care medicine2015

Glibenclamide Improves Survival and Neurologic Outcome After Cardiac Arrest in Rats.

Kaibin Huang, Yong Gu, Yafang Hu, Zhong Ji, Shengnan Wang, Zhenzhou Lin, Xing Li, Zuoshan Xie, Suyue Pan

Abstract read
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In one paragraph

Article in Critical care medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 49 citations in OpenAlex.

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  12. Sulfonylurea Receptor 1 in Central Nervous System Injury: An Updated Review.International journal of molecular sciences · 2021
    Review
  13. Emerging therapeutic targets for cerebral edema.Expert opinion on therapeutic targets · 2021
    Review
  14. Article
  15. Article
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  18. Review
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  20. Glycocalyx degradation leads to blood-brain barrier dysfunction and brain edema after asphyxia cardiac arrest in rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 2 countries.

Kaibin HuangAll authors: Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yong Gu
Yafang Hu
Zhong Ji
Shengnan Wang
Zhenzhou Lin
Xing Li
Zuoshan Xie
Suyue Pan
National Natural Science Foundation of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesGlibenclamide confers neuroprotection in animal models as well as in retrospective clinical studies. This study determines whether glibenclamide improves outcome after cardiac arrest in rats.

designProspective randomized laboratory study.

settingUniversity research laboratory. SUBJECTS: Male Sprague-Dawley rats (n = 126).

interventionsRats successfully resuscitated from 8-minute asphyxial cardiac arrest were randomized to glibenclamide or vehicle group. Rats in the glibenclamide group were intraperitoneally administered glibenclamide with a loading dose of 10 μg/kg at 10 minutes and a maintenance dose of 1.2 μg at 6, 12, 18, and 24 hours after return of spontaneous circulation, whereas rats in the vehicle group received equivalent volume of vehicle solution. MEASUREMENTS AND MAIN

resultsSurvival was recorded every day, and neurologic deficit scores were assessed at 24, 48, and 72 hours and 7 days after return of spontaneous circulation (n = 22 in each group). Results showed that glibenclamide treatment increased 7-day survival rate, reduced neurologic deficit scores, and prevented neuronal loss in the hippocampal cornu ammonis 1 region. To investigate the neuroprotective effects of glibenclamide in acute phase, we observed neuronal injury at 24 hours after return of spontaneous circulation and found that glibenclamide significantly decreased the rate of neuronal necrosis and apoptosis. In addition, glibenclamide reduced the messenger RNA expression of tumor necrosis factor-α and monocyte chemoattractant protein-1 in the cortex after return of spontaneous circulation. Furthermore, the sulfonylurea receptor 1 and transient receptor potential M4 heteromers, the putative therapeutic targets of glibenclamide, were up-regulated after cardiac arrest and cardiopulmonary resuscitation, indicating that they might be involved in neuroprotective effect of glibenclamide.

conclusionsGlibenclamide treatment substantially improved survival and neurologic outcome throughout a 7-day period after return of spontaneous circulation. The salutary effects of glibenclamide were associated with suppression of neuronal necrosis and apoptosis, as well as inflammation in the brain.

Indexed as

AnimalsBrainChemokine CCL2Disease Models, AnimalGlyburideHeart ArrestHemodynamicsMaleNeuroprotective AgentsProspective StudiesRandom AllocationRatsRats, Sprague-DawleyRNA, MessengerSulfonylurea ReceptorsTRPM Cation ChannelsAbcc8 protein, ratChemokine CCL2GlyburideNeuroprotective AgentsRNA, MessengerSulfonylurea ReceptorsTRPM4 protein, ratTRPM Cation ChannelsTumor Necrosis Factor-alpha

Identifiers

PMID26010685
OpenAlexW2323587927

What OpenQuestion holds

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Read underepoch 390

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.