Evidence map›Paper›PMID 31560866›Full record

ReviewArchives of biochemistry and biophysics2019

Carbon monoxide attenuates vasospasm and improves neurobehavioral function after subarachnoid hemorrhage.

Pradip K Kamat, Abdullah S Ahmad, Sylvain Doré

Open access · greenAbstract readReview
In one paragraph

Review in Archives of biochemistry and biophysics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Potential therapeutic effects of Nrf2 activators on intracranial hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Review
  7. Article
  8. Carbon Monoxide: from Poison to Clinical Trials.Trends in pharmacological sciences · 2021
    Review
  9. Review
  10. Observational
  11. Review
  12. Article
  13. Article
  14. 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

3 authors at 2 institutions in 1 country.

Pradip K KamatDepartment of Anesthesiology, United States; Center for Translational Research in Neurodegenerative Disease, University of Florida, United States.
Abdullah S AhmadDepartment of Anesthesiology, United States; Center for Translational Research in Neurodegenerative Disease, University of Florida, United States.
Sylvain DoréDepartment of Anesthesiology, United States; Center for Translational Research in Neurodegenerative Disease, University of Florida, United States; Departments of Neurology, Psychiatry, Pharmaceutics and Neuroscience, McKnight Brain Institute, University of Florida, United States. Electronic address: sdore@ufl.edu.
Institute for Neurodegenerative Disorders · USUniversity of Florida · US

Funding

Regulation and Implication of Hemoglobin Clearance in Subarachnoid Hemorrhagic PatientsR21NS095166 · NINDS · UNIVERSITY OF FLORIDA · PI DORE, SYLVAIN · 2016 to 2017
$426k
CO therapeutic role and potential mechanism in TBIR21NS103036 · NINDS · UNIVERSITY OF FLORIDA · PI DORE, SYLVAIN · 2018 to 2019
$419k
Potential stroke therapeutic efficacy of FumET-CORM through the Nrf2 pathwayR21NS110008 · NINDS · UNIVERSITY OF FLORIDA · PI DORE, SYLVAIN · 2019 to 2019
$419k
NINDS NIH HHS R21 NS095166NINDS NIH HHS R21 NS103036NINDS NIH HHS R21 NS110008
6 · The paper itself

Abstract

Subarachnoid hemorrhage (SAH) is a devastating form of hemorrhagic stroke and is a serious medical condition caused by bleeding usually due to a ruptured aneurysm. Oxidative stress and inflammation from hemoglobin and heme released from lysed red blood cells are some postulated causes of vasospasm during SAH, which could lead to delayed cerebral ischemia. At low amounts, carbon monoxide (CO) gas may be neuroprotective through anti-inflammation, anti-cell death, and restoration of normal blood flow. Hence, this study focuses on a noninvasive strategy to treat SAH by using CO as a therapeutic medical gas. Mice were treated with 250 ppm CO or air for 1h started at 2h after SAH. Various anatomical and functional outcomes were monitored at 1 and 7d after SAH. CO decreased neurological deficit score (47.4 ± 10.5%) and increased activity (30.0 ± 9.1%) and stereotypic counts (261.5 ± 62.1%) at 7d. There was a significant increase in lumen area/wall thickness ratio in the middle cerebral artery (173.5 ± 19.3%), which tended to increase in the anterior cerebral artery (25.5 ± 4.3%) at 7d. This is the first report to demonstrate that CO minimizes delayed SAH-induced neurobehavioral deficits, which suggests that post-treatment with CO gas or CO-donors can be further tested as a potential therapy against SAH.

Indexed as

AnimalsCarbon MonoxideHematomaMaleMice, Inbred C57BLMotor ActivityNeurologySubarachnoid HemorrhageVasospasm, IntracranialCarbon MonoxideDelayed cererbral ischemiaHeme oxygenaseHemorrhagic strokeMedical gasNeurological functionsVasoconstriction

Identifiers

PMID31560866
PMCPMC6917044
OpenAlexW2975301300

What OpenQuestion holds

Textmetadata
LicenceTDM
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.