Evidence map›Paper›PMID 30628008›Full record

ArticleTranslational stroke research2019

The Role of Oxidative Stress in Microvascular Disturbances after Experimental Subarachnoid Hemorrhage.

Toshio Fumoto, Masato Naraoka, Takeshi Katagai, Yuchen Li, Norihito Shimamura, Hiroki Ohkuma

Abstract read
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In one paragraph

Article in Translational stroke research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
10.0field-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

54 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Article
  3. Observational
  4. Review
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  7. Review
  8. Multimodal imaging of the role of hyperglycemia following experimental subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  9. Article
  10. Pathophysiology, Management, and Therapeutics in Subarachnoid Hemorrhage and Delayed Cerebral Ischemia: An Overview.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Review
  11. Article
  12. Role of Estrogen-Related Receptor γ and PGC-1α/SIRT3 Pathway in Early Brain Injury After Subarachnoid Hemorrhage.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Role of hydrogen sulfide in subarachnoid hemorrhage.CNS neuroscience & therapeutics · 2022
    Review
  19. Review
  20. A new perspective on cerebrospinal fluid dynamics after subarachnoid hemorrhage: From normal physiology to pathophysiological changes.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
    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

6 authors at 1 institution in 1 country.

Toshio FumotoDepartment of Neurosurgery, Hirosaki University Graduate School of Medicine, 5 Zaifucho, Hirosaki, Aomori, 036-8562, Japan.
Masato NaraokaDepartment of Neurosurgery, Hirosaki University Graduate School of Medicine, 5 Zaifucho, Hirosaki, Aomori, 036-8562, Japan.
Takeshi KatagaiDepartment of Neurosurgery, Hirosaki University Graduate School of Medicine, 5 Zaifucho, Hirosaki, Aomori, 036-8562, Japan.
Yuchen LiDepartment of Neurosurgery, Hirosaki University Graduate School of Medicine, 5 Zaifucho, Hirosaki, Aomori, 036-8562, Japan.
Norihito ShimamuraDepartment of Neurosurgery, Hirosaki University Graduate School of Medicine, 5 Zaifucho, Hirosaki, Aomori, 036-8562, Japan.
Hiroki OhkumaDepartment of Neurosurgery, Hirosaki University Graduate School of Medicine, 5 Zaifucho, Hirosaki, Aomori, 036-8562, Japan. ohkuma@hirosaki-u.ac.jp.
Hirosaki University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress was shown to play a crucial role in the diverse pathogenesis of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Microcirculatory dysfunction is thought to be an important and fundamental pathological change in EBI. However, other than blood-brain barrier (BBB) disruption, the influence of oxidative stress on microvessels remains to be elucidated. The aim of this study was to investigate the role of oxidative stress on microcirculatory integrity in EBI. SAH was induced in male Sprague-Dawley rats using an endovascular perforation technique. A free radical scavenger, edaravone, was administered prophylactically by intraperitoneal injection. SAH grade, neurological score, brain water content, and BBB permeability were measured at 24 h after SAH induction. In addition, cortical samples taken at 24 h after SAH were analyzed to explore oxidative stress, microvascular mural cell apoptosis, microspasm, and microthrombosis. Edaravone treatment significantly ameliorated neurological deficits, brain edema, and BBB disruption. In addition, oxidative stress-induced modifications and subsequent apoptosis of microvascular endothelial cells and pericytes increased after SAH induction, while the administration of edaravone suppressed this. Consistent with apoptotic cell inhibition, microthromboses were also inhibited by edaravone administration. Oxidative stress plays a pivotal role in the induction of multiple pathological changes in microvessels in EBI. Antioxidants are potential candidates for the treatment of microvascular disturbances after SAH.

Indexed as

AnimalsAntioxidantsBlood-Brain BarrierBrainBrain EdemaBrain InjuriesDisease Models, AnimalEdaravoneMaleMicrocirculationMicrovesselsOxidative StressRatsRats, Sprague-DawleySubarachnoid HemorrhageAntioxidantsEdaravoneEarly brain injuryMicrovesselOxidative stressSubarachnoid hemorrhage

Identifiers

PMID30628008
OpenAlexW2908769754

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.