Evidence map›Paper›PMID 31186479›Full record

ArticleScientific reports2019

Neutrophils mediate early cerebral cortical hypoperfusion in a murine model of subarachnoid haemorrhage.

Axel Neulen, Tobias Pantel, Michael Kosterhon, Andreas Kramer, Sascha Kunath, Maximilian Petermeyer, Bernd Moosmann, Johannes Lotz, Sven R Kantelhardt, Florian Ringel and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Microthrombi and hypercoagulability's contribution to delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  3. Article
  4. The role of neutrophils in vasospasm and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage: Is it time for a SAH clinical trial targeting neutrophils?Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Role of Neutrophils as Therapeutic Targets in Intracerebral Hemorrhage.Therapeutic innovation & regulatory science · 2024
    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

11 authors at 1 institution in 1 country.

Axel NeulenDepartment of Neurosurgery, University Medical Centre of the Johannes Gutenberg-University of Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany. axel.neulen@unimedizin-mainz.de.ORCID http://orcid.org/0000-0003-3547-1630
Tobias PantelDepartment of Neurosurgery, University Medical Centre of the Johannes Gutenberg-University of Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany.
Michael KosterhonDepartment of Neurosurgery, University Medical Centre of the Johannes Gutenberg-University of Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany.
Andreas KramerDepartment of Neurosurgery, University Medical Centre of the Johannes Gutenberg-University of Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany.
Sascha KunathInstitute for Pathobiochemistry, University Medical Centre of the Johannes Gutenberg-University of Mainz, Duesbergweg 6, 55128, Mainz, Germany.
Maximilian PetermeyerDepartment of Neurosurgery, University Medical Centre of the Johannes Gutenberg-University of Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany.
Bernd MoosmannInstitute for Pathobiochemistry, University Medical Centre of the Johannes Gutenberg-University of Mainz, Duesbergweg 6, 55128, Mainz, Germany.
Johannes LotzInstitute for Clinical Chemistry and Laboratory Medicine, University Medical Centre of the Johannes Gutenberg-University of Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany.
Sven R KantelhardtDepartment of Neurosurgery, University Medical Centre of the Johannes Gutenberg-University of Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany.
Florian RingelDepartment of Neurosurgery, University Medical Centre of the Johannes Gutenberg-University of Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany.
Serge C ThalDepartment of Anaesthesiology, University Medical Centre of the Johannes Gutenberg-University of Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany. thal@uni-mainz.de.ORCID http://orcid.org/0000-0002-1222-8729
Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral hypoperfusion in the first hours after subarachnoid haemorrhage (SAH) is a major determinant of poor neurological outcome. However, the underlying pathophysiology is only partly understood. Here we induced neutropenia in C57BL/6N mice by anti-Ly6G antibody injection, induced SAH by endovascular filament perforation, and analysed cerebral cortical perfusion with laser SPECKLE contrast imaging to investigate the role of neutrophils in mediating cerebral hypoperfusion during the first 24 h post-SAH. SAH induction significantly increased the intracranial pressure (ICP), and significantly reduced the cerebral perfusion pressure (CPP). At 3 h after SAH, ICP had returned to baseline and CPP was similar between SAH and sham mice. However, in SAH mice with normal neutrophil counts cortical hypoperfusion persisted. Conversely, despite similar CPP, cortical perfusion was significantly higher at 3 h after SAH in mice with neutropenia. The levels of 8-iso-prostaglandin-F2α in the subarachnoid haematoma increased significantly at 3 h after SAH in animals with normal neutrophil counts indicating oxidative stress, which was not the case in neutropenic SAH animals. These results suggest that neutrophils are important mediators of cortical hypoperfusion and oxidative stress early after SAH. Targeting neutrophil function and neutrophil-induced oxidative stress could be a promising new approach to mitigate cerebral hypoperfusion early after SAH.

Indexed as

AnimalsAntibodies, Anti-IdiotypicAntigens, LyBlood PressureCerebral CortexCerebrovascular CirculationDisease Models, AnimalHumansIntracranial PressureMaleMiceMice, Inbred C57BLNeutropeniaNeutrophilsSubarachnoid HemorrhageAntibodies, Anti-IdiotypicAntigens, LyLy6G antigen, mouse

Identifiers

PMID31186479
PMCPMC6560094
OpenAlexW2952788645

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.