Evidence map›Paper›PMID 29299201›Full record

ArticleIranian journal of basic medical sciences2017

Acute sleep deprivation preconditions the heart against ischemia/ reperfusion injury: the role of central GABA-A receptors.

Hoda Parsa, Alireza Imani, Mahdieh Faghihi, Esmail Riahi, Mohammad Badavi, Abbas Shakoori, Tayebeh Rastegar, Marjan Aghajani, Sulail Fatima Rajani

Open access · greenAbstract read
In one paragraph

Article in Iranian journal of basic medical sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 12 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

9 authors at 2 institutions in 1 country.

Hoda ParsaDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Alireza ImaniDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mahdieh FaghihiDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Esmail RiahiDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mohammad BadaviDepartment of Physiology, School of Medicine, Ahwaz University of Medical Sciences, Ahwaz, Iran.
Abbas ShakooriDepartment of Genetic, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Tayebeh RastegarDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Marjan AghajaniDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Sulail Fatima RajaniDepartment of Physiology, School of Medicine, Tehran University of Medical Sciences, International Campus, Tehran, Iran.
Tehran University of Medical Sciences · IRAhvaz Jundishapur University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesCentral γ-aminobutyric acid (GABA) neurotransmission modulates cardiovascular functions and sleep. Acute sleep deprivation (ASD) affects functions of various body organs via different mechanisms. Here, we evaluated the effect of ASD on cardiac ischemia/reperfusion injury (IRI), and studied the role of GABA-A receptor inhibition in central nucleus of amygdala (CeA) by assessing nitric oxide (NO) and oxidative stress. MATERIALS AND

methodsThe CeA in sixty male Wistar rats was cannulated for saline or bicuculline (GABA-A receptor antagonist) administration. All animals underwent 30 min of coronary occlusion (ischemia), followed by 2 hr reperfusion (IR). The five experimental groups (n=12) included are as follows: IR: received saline; BIC+IR: received Bicuculline; MLP+IR: received saline, followed by the placement of animals in an aquarium with multiple large platforms; ASD+IR: underwent ASD in an aquarium with multiple small platforms; and BIC+ASD+IR: received bicuculline prior to ASD.

resultsBicuculline administration increased the malondialdehyde levels and infarct size, and decreased the NO metabolites levels and endothelial nitric oxide synthase (eNOS) gene expression in infarcted and non-infarcted areas in comparison to IR group. ASD reduced malondialdehyde levels and infarct size and increased NO metabolites, corticosterone levels and eNOS expression in infarcted and non-infarcted areas as compared to the IR group. Levels of malondialdehyde were increased while levels of NO metabolites, corticosterone and eNOS expression in infarcted and non-infarcted areas were reduced in the BIC+ASD+IR as compared to the ASD+IR group.

conclusionBlockade of GABA-A receptors in the CeA abolishes ASD-induced cardioprotection by suppressing oxidative stress and NO production.

Indexed as

Acute sleep deprivationBicucullineGABA-A receptorInfarct sizeMyocardial ischemia/-reperfusionNitric oxide

Identifiers

PMID29299201
PMCPMC5749358
OpenAlexW2766961792

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.