Evidence map›Paper›PMID 29843508›Full record

ArticleKorean journal of anesthesiology2019

Dexmedetomidine and propofol sedation requirements in an autistic rat model.

Soha A Elmorsy, Ghada F Soliman, Laila A Rashed, Hamed Elgendy

Open access · goldAbstract read
In one paragraph

Article in Korean journal of anesthesiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Trial
  2. 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

4 authors at 2 institutions in 2 countries.

Soha A ElmorsyDepartment of Medical Pharmacology, Cairo University Faculty of Medicine, Qatar.
Ghada F SolimanDepartment of Medical Pharmacology, Cairo University Faculty of Medicine, Qatar.
Laila A RashedDepartment of Medical Biochemistry, Cairo University Faculty of Medicine, Qatar.
Hamed ElgendyDepartment of Anesthesia, Assiut University Hospital, Egypt & Hamad Medical Corporation, Weill Cornell Medicine-Qatar, Doha, Qatar.
Cairo University · EGHamad General Hospital · QA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutism is a challenging neurodevelopmental disorder. Previous clinical observations have suggested altered sedation requirements for children with autism. Our study aimed to test this observation experimentally in an animal model and to explore its possible mechanisms.

methodsEight adult pregnant female Sprague-Dawley rats were randomly divided into two groups. Four were injected with intraperitoneal sodium valproate on gestational day 12 and four were injected with normal saline. On postnatal day 28, the newborn male rats were subjected to the open-field test to confirm autistic features. Each rat was injected intraperitoneally with a single dose of propofol (50 mg/kg) or dexmedetomidine (0.2 mg/kg). The times to loss of righting reflex (LORR) and to return of righting reflex (RORR) were recorded. On the following day, all rats were re-sedated and underwent electroencephalography (EEG). Thereafter, the rats were euthanized and their hippocampal gamma-aminobutyric acid type A (GABAA) and glutamate N-methyl-D-aspartate (NMDA) receptor gene expressions were assessed.

resultsAutistic rats showed significantly longer LORR times and shorter RORR times than did the controls (median LORR times: 12.0 versus 5.0 min for dexmedetomidine and 22.0 versus 8.0 min for propofol; P < 0.05). EEG showed a low-frequency, high-amplitude wave pattern 2 min after LORR in the control rats. Autistic rats showed a high-frequency, low-amplitude awake pattern. Hippocampal GABAA receptor gene expression was significantly lower and NMDA gene expression was greater in autistic rats.

conclusionsThis study supports the clinical observations of increased anesthetic sedative requirements in children with autism and our biochemical analyses using GABAA and glutamate receptor gene expression highlight possible underlying mechanisms.

Indexed as

Disease Models, AnimalAnimalsAnimals, NewbornAutistic DisorderDexmedetomidineElectroencephalographyFemaleHypnotics and SedativesMalePregnancyPropofolRandom AllocationRatsRats, Sprague-DawleyDexmedetomidineHypnotics and SedativesPropofolAutismDexmedetomidineGABAAGlutamatePropofol

Identifiers

PMID29843508
PMCPMC6458507
OpenAlexW2807353439

What OpenQuestion holds

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LicenceCC BY-NC
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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.