Evidence map›Paper›PMID 34855119›Full record

ArticleNeurocritical care2022

Transient Hypoperfusion to Ischemic/Anoxic Spreading Depolarization is Related to Autoregulatory Failure in the Rat Cerebral Cortex.

Ákos Menyhárt, Dániel Péter Varga, Orsolya M Tóth, Péter Makra, Ferenc Bari, Eszter Farkas

Open access · hybridAbstract read
In one paragraph

Article in Neurocritical care, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

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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

6 authors at 1 institution in 2 countries.

Ákos MenyhártDepartment of Medical Physics and Informatics, Faculty of Science and Informatics, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Dániel Péter VargaDepartment of Medical Physics and Informatics, Faculty of Science and Informatics, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Orsolya M TóthDepartment of Medical Physics and Informatics, Faculty of Science and Informatics, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Péter MakraDepartment of Medical Physics and Informatics, Faculty of Science and Informatics, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Ferenc BariDepartment of Medical Physics and Informatics, Faculty of Science and Informatics, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Eszter FarkasCerebral Blood Flow and Metabolism Research Group, Hungarian Centre of Excellence for Molecular Medicine, University of Szeged, Szeged, Hungary. eszter.farkas@hcemm.eu.ORCID 0000-0002-8478-9664
University of Szeged · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn ischemic stroke, cerebral autoregulation and neurovascular coupling may become impaired. The cerebral blood flow (CBF) response to spreading depolarization (SD) is governed by neurovascular coupling. SDs recur in the ischemic penumbra and reduce neuronal viability by the insufficiency of the CBF response. Autoregulatory failure and SD may coexist in acute brain injury. Here, we set out to explore the interplay between the impairment of cerebrovascular autoregulation, SD occurrence, and the evolution of the SD-coupled CBF response.

methodsIncomplete global forebrain ischemia was created by bilateral common carotid artery occlusion in isoflurane-anesthetized rats, which induced ischemic SD (iSD). A subsequent SD was initiated 20-40 min later by transient anoxia SD (aSD), achieved by the withdrawal of oxygen from the anesthetic gas mixture for 4-5 min. SD occurrence was confirmed by the recording of direct current potential together with extracellular K

resultsIschemia induction and anoxia onset gave rise to iSD and aSD, respectively, albeit aSD occurred at a longer latency, and was superimposed on a gradual elevation of K

conclusionsWe propose that the dysfunction of cerebrovascular autoregulation that occurs simultaneously with hypotension transients poses a substantial risk of SD occurrence and is not a consequence of SD. Under such circumstances, the evolving SD is not accompanied by any recognizable CBF response, which indicates a severely damaged neurovascular coupling.

Indexed as

Cerebrovascular CirculationHypotensionAnimalsCerebral CortexHomeostasisHypoxiaIschemiaRatsCerebral blood flowCerebrovascular autoregulationIschemic strokeNeurovascular couplingSpreading depolarizationSpreading ischemia

Identifiers

PMID34855119
PMCPMC9259535
OpenAlexW3215287834

What OpenQuestion holds

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Registered trials

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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.