Evidence map›Paper›PMID 23188422›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2013

Inhaled nitric oxide reduces secondary brain damage after traumatic brain injury in mice.

Nicole A Terpolilli, Seong-Woong Kim, Serge C Thal, Wolfgang M Kuebler, Nikolaus Plesnila

2 registry-linked trialsOpen 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, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 4% 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.

NCT03260569 phase3completednot on this mapstarted 2018, after this paper: background citation

Respiratory Mechanics Following Brain Injury: The Role of Inhaled Nitric Oxide

TypeinterventionalSponsorUniversity of CincinnatiRan2018 to 2023Enrolled13ConditionsTraumatic Brain InjuryArmsInhaled Nitric Oxide, Placebo
NCT04988932 nacompletednot on this map

Inhalative Stickstoffmonoxid (NO) Behandlung Bei Patienten Mit Schwerem, therapierefraktärem Zerebralen Vasospasmus Nach Subarachnoidalblutung

TypeinterventionalSponsorInsel Gruppe AG, University Hospital BernRan2012 to 2020Enrolled7ConditionsSAH, Inhaled Nitric Oxide, Cerebral Ischemia, VasospasmArmsInhaled nitric oxide
3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Nitric oxide and traumatic brain injury.Medical gas research · 2027
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
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  10. Article
  11. Phosphodiesterase-5 (PDE-5) Inhibitors as Therapy for Cerebrovascular Dysfunction in Chronic Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  12. Article
  13. Inhaled Nitric Oxide Promotes Angiogenesis in the Rodent Developing Brain.International journal of molecular sciences · 2023
    Article
  14. Review
  15. Review
  16. Review
  17. CaeLife · 2022
    Article
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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

5 authors at 1 institution in 1 country.

Nicole A TerpolilliDepartment of Neurosurgery, University of Munich Medical Center, Munich, Germany.
Seong-Woong Kim
Serge C Thal
Wolfgang M Kuebler
Nikolaus Plesnila
Ludwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia, especially pericontusional ischemia, is one of the leading causes of secondary brain damage after traumatic brain injury (TBI). So far efforts to improve cerebral blood flow (CBF) after TBI were not successful because of various reasons. We previously showed that nitric oxide (NO) applied by inhalation after experimental ischemic stroke is transported to the brain and induces vasodilatation in hypoxic brain regions, thus improving regional ischemia, thereby improving brain damage and neurological outcome. As regional ischemia in the traumatic penumbra is a key mechanism determining secondary posttraumatic brain damage, the aim of the current study was to evaluate the effect of NO inhalation after experimental TBI. NO inhalation significantly improved CBF and reduced intracranial pressure after TBI in male C57 Bl/6 mice. Long-term application (24 hours NO inhalation) resulted in reduced lesion volume, reduced brain edema formation and less blood-brain barrier disruption, as well as improved neurological function. No adverse effects, e.g., on cerebral auto-regulation, systemic blood pressure, or oxidative damage were observed. NO inhalation might therefore be a safe and effective treatment option for TBI patients.

Indexed as

AnimalsBlood-Brain BarrierBlood PressureBrain EdemaBrain InjuriesBrain IschemiaCerebrovascular CirculationDisease Models, AnimalEndothelium-Dependent Relaxing FactorsHumansMaleMiceNitric OxideEndothelium-Dependent Relaxing FactorsNitric Oxide

Identifiers

PMID23188422
PMCPMC3564204
OpenAlexW2015642857

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.