Evidence map›Paper›PMID 24865999›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2014

CO2 has no therapeutic effect on early microvasospasm after experimental subarachnoid hemorrhage.

Benjamin Friedrich, Radoslaw Michalik, Anna Oniszczuk, Khalid Abubaker, Ewa Kozniewska, Nikolaus Plesnila

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Article
  7. Long-term impairment of neurovascular coupling following experimental subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Article
  8. High-normal PBMC neurology · 2020
    Article
  9. Lesional and perilesional tissue characterization by automated image processing in a novel gyrencephalic animal model of peracute intracerebral hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Carbonic anhydrase inhibitors modify intracellular pH transients and contractions of rat middle cerebral arteries during COJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Article
  14. Inversion of neurovascular coupling after subarachnoid hemorrhage in vivo.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Article
  15. Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Article
  16. Nitric oxide inhalation reduces brain damage, prevents mortality, and improves neurological outcome after subarachnoid hemorrhage by resolving early pial microvasospasms.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016
    Article
  17. Article
  18. Dysfunction of mouse cerebral arteries during early aging.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015
    Article
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 3 institutions in 3 countries.

Benjamin FriedrichInstitute for Surgical Research, University of Munich Medical Center, Munich, Germany.
Radoslaw MichalikDepartment of Neurooncology, The Maria Skłodowska-Curie Memorial Center and Institute of Oncology, Warsaw, Poland.
Anna OniszczukDepartment of Neurosurgery, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
Khalid AbubakerRoyal College of Surgeons in Ireland, Dublin, Ireland.
Ewa KozniewskaDepartment of Neurosurgery, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
Nikolaus Plesnila1] Institute for Surgical Research, University of Munich Medical Center, Munich, Germany [2] Royal College of Surgeons in Ireland, Dublin, Ireland [3] Institute for Stroke and Dementia Research, University of Munich Medical Center, Munich, Germany.
Polish Academy of Sciences · PLRoyal College of Surgeons in Ireland · IEThe Maria Sklodowska-Curie National Research Institute of Oncology · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to delayed vasospasm also early brain injury, which occurs during the first few days after subarachnoid hemorrhage (SAH) when large cerebral arteries are still fully functional, plays an important role for the outcome after SAH. In the current study, we investigated the hypothesis that carbon dioxide (CO2), a strong cerebral vasodilator, has a therapeutic potential against early posthemorrhagic microvasospasm. C57BL/6 mice (n=36) and Sprague-Dawley rats (n=23) were subjected to sham surgery or SAH by filament perforation. The pial microcirculation in the mice was visualized 3 and 24 hours after SAH using intravital fluorescence microscopy. Partial pressure of CO2 (PaCO2) was modulated by hyper- or hypoventilation or by inhalation of 10% CO2. In rats, CO2-mediated changes in cerebral blood flow (CBF) were measured at the same time points using laser Doppler fluxmetry. Increased PaCO2 caused vasodilatation in sham-operated animals. Following SAH, however, cerebral arterioles were nonreactive to CO2. This lack of microvascular CO2 reactivity was accompanied by a complete loss of CO2-induced hyperemia. Our data show that CO2 is not able to dilate spastic microvessels and to increase CBF early after SAH. Future therapeutic approaches will therefore need to address mechanisms beyond CO2.

Indexed as

Administration, InhalationAnimalsBlood Flow VelocityCarbon DioxideCerebral ArteriesCerebrovascular CirculationDisease Models, AnimalLaser-Doppler FlowmetryMaleMiceMice, Inbred C57BLMicroscopy, FluorescenceMicrovesselsRatsRats, Sprague-DawleySubarachnoid HemorrhageCarbon Dioxide

Identifiers

PMID24865999
PMCPMC4126102
OpenAlexW2072298474

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.