Evidence map›Paper›PMID 27044361›Full record

ArticleTranslational stroke research2016

Role of Cyclooxygenase-2 in Relation to Nitric Oxide and Endothelin-1 on Pathogenesis of Cerebral Vasospasm After Subarachnoid Hemorrhage in Rabbit.

Akira Munakata, Masato Naraoka, Takeshi Katagai, Norihito Shimamura, Hiroki Ohkuma

Abstract read
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In one paragraph

Article in Translational stroke research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 3 pooled it
4.0field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 3 syntheses or guidelines pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Haemorrhage, hypercoagulability and ischaemia: Evolution of brain injury after aneurysmal subarachnoid haemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  5. Review
  6. Review
  7. Emerging therapeutic targets for cerebral edema.Expert opinion on therapeutic targets · 2021
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. PDGFR-β modulates vascular smooth muscle cell phenotype via IRF-9/SIRT-1/NF-κB pathway in subarachnoid hemorrhage rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Article
  14. Anti-inflammation conferred by stimulation of CD200R1 via Dok1 pathway in rat microglia after germinal matrix hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Article
  15. Review
  16. Neural regeneration research · 2018
    Article
  17. Review
  18. Review
  19. 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

5 authors at 1 institution in 1 country.

Akira MunakataDepartment of Neurosurgery, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki-shi, Aomori-ken, 036-8562, Japan.
Masato NaraokaDepartment of Neurosurgery, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki-shi, Aomori-ken, 036-8562, Japan.
Takeshi KatagaiDepartment of Neurosurgery, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki-shi, Aomori-ken, 036-8562, Japan.
Norihito ShimamuraDepartment of Neurosurgery, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki-shi, Aomori-ken, 036-8562, Japan.
Hiroki OhkumaDepartment of Neurosurgery, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki-shi, Aomori-ken, 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

Endothelial dysfunctions that include decreased nitric oxide (NO) bioactivity and increased endothelin-1 (ET-1) bioactivity have been considered to be involved in the pathogenesis of cerebral vasospasm (CVS) after aneurysmal subarachnoid hemorrhage (SAH). Recent cardiovascular studies have revealed that cyclooxygenase-2 (COX-2) is involved in a disturbance in cross-talk between NO and ET-1. COX-2 expression was detected in the endothelial cells of a spastic artery after experimental SAH; however, the pathophysiological significance of COX-2 in relation to CVS remains unclear. The aim of this study was to investigate the role of COX-2 in relation to NO and ET-1 in the pathogenesis of CVS by using the COX-2 selective inhibitor, celecoxib. In the SAH group, SAH was simulated using the double-hemorrhage rabbit model. In the celecoxib group, SAH was simulated and celecoxib was administered. The basilar artery was extracted on day 5 and examined. The cross-section area of the basilar artery in the celecoxib group was significantly larger than in the SAH group. An increased expression of COX-2, ET-1, and ETA receptor (ETAR), and a decreased expression of endothelial NO synthase (eNOS) were seen in the SAH group. In the celecoxib group compared to the SAH group, expression of COX-2, ET-1, and ETAR were statistically significantly decreased, and eNOS expression was significantly increased. COX-2 might be involved in the pathogenesis of CVS due to up-regulation of ET-1 and ETAR and down-regulation of eNOS, and celecoxib may potentially serve as an agent in the prevention of CVS after SAH.

Indexed as

AnimalsCyclooxygenase 2Disease Models, AnimalEndothelin-1Nitric OxideRabbitsSubarachnoid HemorrhageUp-RegulationVasospasm, IntracranialCyclooxygenase 2Endothelin-1Nitric OxideCelecoxibCerebral vasospasmCyclooxygenase-2Endothelin-1Nitric oxideSubarachnoid hemorrhage

Identifiers

PMID27044361
OpenAlexW2340011231

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.