Evidence map›Paper›PMID 35567916›Full record

ArticleAutonomic neuroscience : basic & clinical2022

Sympathetic nervous system hyperactivity results in potent cerebral hypoperfusion in swine.

Wi Jin Kim, Michael Dacey, Hashitha Milan Samarage, David Zarrin, Keshav Goel, Christopher Chan, Xin Qi, Anthony C Wang, Kalyanam Shivkumar, Jeffrey Ardell and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Autonomic neuroscience : basic & clinical, 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
1.4field-weighted citation impact, top 21% 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, 11 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

11 authors at 1 institution in 1 country.

Wi Jin KimDepartment of Neurosurgery, University of California Los Angeles, Los Angeles, CA, USA.
Michael DaceyCardiac Arrhythmia Center, Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Hashitha Milan SamarageDepartment of Neurosurgery, University of California Los Angeles, Los Angeles, CA, USA.
David ZarrinDavid Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Keshav GoelDavid Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Christopher ChanCardiac Arrhythmia Center, Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Xin QiDavid Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Anthony C WangDepartment of Neurosurgery, University of California Los Angeles, Los Angeles, CA, USA.
Kalyanam ShivkumarCardiac Arrhythmia Center, Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Jeffrey ArdellCardiac Arrhythmia Center, Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Geoffrey P ColbyDepartment of Neurosurgery, University of California Los Angeles, Los Angeles, CA, USA. Electronic address: gcolby@mednet.ucla.edu.
University of California, Los Angeles · US

Funding

UCLA Neurosurgery Research Training and Education ProgramR25NS079198 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LIAU, LINDA M · 2012 to 2021
$1.2M
NINDS NIH HHS R25 NS079198
6 · The paper itself

Abstract

introductionCerebral vasospasm is a complex disease resulting in reversible narrowing of blood vessels, stroke, and poor patient outcomes. Sympathetic perivascular nerve fibers originate from the superior cervical ganglion (SCG) to innervate the cerebral vasculature, with activation resulting in vasoconstriction. Sympathetic pathways are thought to be a significant contributor to cerebral vasospasm.

objectiveWe sought to demonstrate that stimulation of SCG in swine can cause ipsilateral cerebral perfusion deficit similar to that of significant human cerebral vasospasm. Furthermore, we aimed to show that inhibition of SCG can block the effects of sympathetic-mediated cerebral hypoperfusion.

methodsSCG were surgically identified in 15 swine and were electrically stimulated to achieve sympathetic activation. CT perfusion scans were performed to assess for changes in cerebral blood flow (CBF), cerebral blood volume (CBV), mean transit time (MTT) and time-to-maximum (TMax). Syngo.via software was used to determine regions of interest and quantify perfusion measures.

resultsSCG stimulation resulted in 20-30% reduction in mean ipsilateral CBF compared to its contralateral unaffected side (p < 0.001). Similar results of hypoperfusion were seen with CBV, MTT and TMax with SCG stimulation. Prior injection of lidocaine to SCG inhibited the effects of SCG stimulation and restored perfusion comparable to baseline (p > 0.05).

conclusionIn swine, SCG stimulation resulted in significant cerebral perfusion deficit, and this was inhibited by prior local anesthetic injection into the SCG. Inhibiting sympathetic activation by targeting the SCG may be an effective treatment for sympathetic mediated cerebral hypoperfusion.

Indexed as

Vasospasm, IntracranialAnimalsCerebrovascular CirculationSuperior Cervical GanglionSwineSympathetic Nervous SystemCerebral hypoperfusionCerebral vasospasmSCGSuperior cervical gangliaSympathetic cerebral vasoconstrictionVasospasm

Identifiers

PMID35567916
PMCPMC9659432
OpenAlexW4229013511

What OpenQuestion holds

Textmetadata
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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.