Evidence map›Paper›PMID 27774520›Full record

ArticleBrain circulation2016

Inducible nitric oxide synthase (NOS-2) in subarachnoid hemorrhage: Regulatory mechanisms and therapeutic implications.

Sana Iqbal, Erik G Hayman, Caron Hong, Jesse A Stokum, David B Kurland, Volodymyr Gerzanich, J Marc Simard

Registry-linked trialOpen access · diamondAbstract read
In one paragraph

Article in Brain circulation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05686265 (Cerebral Nitrosative/Oxidative Stress in Aneurysmal Subarachnoid Haemorrhage), which is not on this map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 10% 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.

NCT05686265 terminatednot on this mapstarted 2023, after this paper: background citation

Cerebral Nitrosative/Oxidative Stress in Aneurysmal Subarachnoid Haemorrhage

TypeobservationalSponsorRigshospitalet, DenmarkRan2023 to 2024Enrolled3ConditionsSubarachnoid Hemorrhage, AneurysmalArmsOxygen
3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. 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
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  5. Role of perivascular and meningeal macrophages in outcome following experimental subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
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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

7 authors at 1 institution in 1 country.

Sana IqbalDepartment of Neurosurgery, School of Medicine, University of Maryland, Baltimore, Maryland, USA.
Erik G HaymanDepartment of Neurosurgery, School of Medicine, University of Maryland, Baltimore, Maryland, USA.
Caron HongDepartment of Anesthesiology, School of Medicine, University of Maryland, Baltimore, Maryland, USA.
Jesse A StokumDepartment of Neurosurgery, School of Medicine, University of Maryland, Baltimore, Maryland, USA.
David B KurlandDepartment of Neurosurgery, School of Medicine, University of Maryland, Baltimore, Maryland, USA.
Volodymyr GerzanichDepartment of Neurosurgery, School of Medicine, University of Maryland, Baltimore, Maryland, USA.
J Marc SimardDepartment of Neurosurgery, School of Medicine, University of Maryland, Baltimore, Maryland, USA; Department of Pathology, School of Medicine, University of Maryland, Baltimore, Maryland, USA; Department of Physiology, School of Medicine, University of Maryland, Baltimore, Maryland, USA.
University of Maryland, Baltimore · US

Funding

Sulfonylurea receptor 1 (SUR1)- A novel therapeutic target in ischemic strokeR01HL082517 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI SIMARD, J. MARC · 2006 to 2021
$5.6M
Pathological role of the SUR1-regulated NC(Ca-ATP) channel in cortex after subaraR01NS061808 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI SIMARD, J. MARC · 2009 to 2013
$1.6M
NHLBI NIH HHS R01 HL082517NINDS NIH HHS R01 NS061808
6 · The paper itself

Abstract

Aneurysmal subarachnoid hemorrhage (SAH) typically carries a poor prognosis. Growing evidence indicates that overabundant production of nitric oxide (NO) may be responsible for a large part of the secondary injury that follows SAH. Although SAH modulates the activity of all three isoforms of nitric oxide synthase (NOS), the inducible isoform, NOS-2, accounts for a majority of NO-mediated secondary injuries after SAH. Here, we review the indispensable physiological roles of NO that must be preserved, even while attempting to downmodulate the pathophysiologic effects of NO that are induced by SAH. We examine the effects of SAH on the function of the various NOS isoforms, with a particular focus on the pathological effects of NOS-2 and on the mechanisms responsible for its transcriptional upregulation. Finally, we review interventions to block NOS-2 upregulation or to counteract its effects, with an emphasis on the potential therapeutic strategies to improve outcomes in patients afflicted with SAH. There is still much to be learned regarding the apparently maladaptive response of NOS-2 and its harmful product NO in SAH. However, the available evidence points to crucial effects that, on balance, are adverse, making the NOS-2/NO/peroxynitrite axis an attractive therapeutic target in SAH.

Indexed as

Heparinnitric oxide (NO)NOS-1NOS-2NOS-3subarachnoid hemorrhage (SAH)

Identifiers

PMID27774520
PMCPMC5074544
OpenAlexW2462649220

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.