Evidence map›Paper›PMID 26932203›Full record

ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2016

Dexmedetomidine Postconditioning Reduces Brain Injury after Brain Hypoxia-Ischemia in Neonatal Rats.

Xiaoyan Ren, Hong Ma, Zhiyi Zuo

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
20.3field-weighted citation impact, top 1% 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

33 citing papers in PubMed, 68 citations in OpenAlex.

  1. Trial
  2. Article
  3. Dexmedetomidine alleviates blood-brain barrier disruption in rats after cerebral ischemia-reperfusion by suppressing JNK and p38 MAPK signaling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  4. Article
  5. Alpha-adrenergic receptor activation after fetal hypoxia-ischaemia suppresses transient epileptiform activity and limits loss of oligodendrocytes and hippocampal neurons.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Article
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  7. Review
  8. Article
  9. Review
  10. Article
  11. Dexmedetomidine versus intermittent morphine for sedation of neonates with encephalopathy undergoing therapeutic hypothermia.Journal of perinatology : official journal of the California Perinatal Association · 2021
    Observational
  12. Article
  13. Article
  14. Article
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  18. Curcumin targets vascular endothelial growth factorThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020
    Article
  19. An αInternational journal of medical sciences · 2020
    Article
  20. Review
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

3 authors at 2 institutions in 2 countries.

Xiaoyan RenDepartment of Anesthesiology, University of Virginia, Charlottesville, VA, 22908, USA.
Hong MaDepartment of Anesthesiology, First Hospital of China Medical University, Shenyang, 110001, People's Republic of China. mahong5466@yahoo.com.
Zhiyi ZuoDepartment of Anesthesiology, University of Virginia, Charlottesville, VA, 22908, USA. zz3c@virginia.edu.
First Hospital of China Medical University · CNUniversity of Virginia · US

Funding

Volatile anesthetic effects on aging brainR01GM098308 · NIGMS · UNIVERSITY OF VIRGINIA · PI ZUO, ZHIYI · 2012 to 2015
$1.2M
NIGMS NIH HHS R01 GM098308
6 · The paper itself

Abstract

Perinatal asphyxia can lead to death and severe disability. Brain hypoxia-ischemia (HI) injury is the major pathophysiology contributing to death and severe disability after perinatal asphyxia. Here, seven-day old Sprague-Dawley rats were subjected to left brain HI. Dexmedetomidine was given intraperitoneally after the brain HI. Yohimbine or atipamezole, two α2 adrenergic receptor antagonists, were given 10 min before the dexmedetomidine injection. Neurological outcome was evaluated 7 or 28 days after the brain HI. Frontal cerebral cortex was harvested 6 h after the brain HI. Left brain HI reduced the left cerebral hemisphere weight assessed 7 days after the brain HI. This brain tissue loss was dose-dependently attenuated by dexmedetomidine. Dexmedetomidine applied within 1 h after the brain HI produced this effect. Dexmedetomidine attenuated the brain HI-induced brain tissue and cell loss as well as neurological and cognitive dysfunction assessed from 28 days after the brain HI. Dexmedetomidine postconditioning-induced neuroprotection was abolished by yohimbine or atipamezole. Brain HI increased tumor necrosis factor α and interleukin 1β in the brain tissues. This increase was attenuated by dexmedetomidine. Atipamezole inhibited this dexmedetomidine effect. Our results suggest that dexmedetomidine postconditioning reduces HI-induced brain injury in the neonatal rats. This effect may be mediated by α2 adrenergic receptor activation that inhibits inflammation in the ischemic brain tissues.

Indexed as

Adrenergic alpha-2 Receptor AgonistsAnimalsAnimals, NewbornBrain InjuriesCerebral CortexDexmedetomidineDose-Response Relationship, DrugHypoxia-Ischemia, BrainIschemic PostconditioningMaze LearningNeuroprotective AgentsRatsRats, Sprague-DawleyAdrenergic alpha-2 Receptor AgonistsDexmedetomidineNeuroprotective AgentsDexmedetomidineNeonatesNeuroprotectionPostconditioningRatsα2 adrenergic receptors

Identifiers

PMID26932203
OpenAlexW2289816811

What OpenQuestion holds

Textmetadata
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.