Evidence map›Paper›PMID 22890664›Full record

ArticleActa neurochirurgica. Supplement2013

Subarachnoid blood converts neurally evoked vasodilation to vasoconstriction in rat brain cortex.

Masayo Koide, Adrian D Bonev, Mark T Nelson, George C Wellman

Open access · greenAbstract read
In one paragraph

Article in Acta neurochirurgica. Supplement, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
5.8field-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.

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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
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  11. Dysregulation of oxygen hemodynamic responses to synaptic train stimulation in a rat hippocampal model of subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016
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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

4 authors at 1 institution in 1 country.

Masayo KoideDepartment of Pharmacology, University of Vermont College of Medicine, Burlington, VT 05405-0068, USA.
Adrian D Bonev
Mark T Nelson
George C Wellman
University of Vermont · US

Funding

Impact of SAH on Parenchymal Arterioles and Neurovascular CouplingP01HL095488 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BONEV, ADRIAN · 2010 to 2014
$11.4M
Center for Neuroscience ExcellenceP30GM103498 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI PARSONS, RODNEY L · 2012 to 2015
$4.3M
REGULATION OF CEREBRAL ARTERY DILATIONR01HL044455 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI NELSON, MARK T · 1991 to 2010
$3.9M
Cerebral artery Ca2+ signaling &subarachnoid hemorrhageR01HL078983 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI WELLMAN, GEORGE C · 2005 to 2009
$2.0M
NHLBI NIH HHS P01 HL095488NHLBI NIH HHS R01 HL044455NHLBI NIH HHS R01 HL078983NHLBI NIH HHS R01 HL078983-05 S1NIGMS NIH HHS P30 GM103498
6 · The paper itself

Abstract

The matching of blood flow to regional brain function, called functional hyperemia or neurovascular coupling, involves the coordinated activity of neurons, astrocytes, and parenchymal arterioles. Under physiological conditions, localized neuronal activation leads to elevated astrocyte endfoot Ca(2+) and vasodilation, resulting in an increase in cerebral blood flow. In this study, we examined the impact of subarachnoid hemorrhage (SAH) on neurovascular coupling. SAH model rats received two injections of autologous blood into the cisterna magna 24 h apart. Cortical brain slices from SAH model animals were prepared 4 days after the initial blood injection. Arteriolar diameter and astrocyte endfoot Ca(2+) were simultaneously measured using two-photon microscopy. As expected, neuronal activity evoked by electrical field stimulation (EFS) caused an elevation in endfoot Ca(2+) and vasodilation in brain slices from control animals. However, in brain slices from SAH animals, EFS induced a similar increase in astrocyte endfoot Ca(2+) that caused arteriolar constriction rather than vasodilation. Vasoconstriction was observed in approximately 90% of brain slices from SAH animals in response to EFS, with 40% exhibiting a sustained vasoconstriction, 30% exhibiting a transient vasoconstriction -(diameter restored within 1 min after EFS), and 20% responded with a biphasic response (brief vasodilation followed by -vasoconstriction). This inversion of neurovascular coupling may play a role in the development of neurological deficits following SAH.

Indexed as

AnimalsCalciumCerebral CortexCerebrovascular CirculationDisease Models, AnimalElectric StimulationEvoked PotentialsIn Vitro TechniquesMaleRatsRats, Sprague-DawleySubarachnoid HemorrhageVasoconstrictionVasodilationCalcium

Identifiers

PMID22890664
PMCPMC3684063
OpenAlexW200427905

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.