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

Cerebral hypoperfusion Cerebral vasospasm SCG Superior cervical ganglia Sympathetic cerebral vasoconstriction Vasospasm

Journal

Autonomic neuroscience : basic & clinical
ISSN: 1872-7484
Titre abrégé: Auton Neurosci
Pays: Netherlands
ID NLM: 100909359

Informations de publication

Date de publication:
09 2022
Historique:
received: 29 12 2021
revised: 14 04 2022
accepted: 04 05 2022
pubmed: 15 5 2022
medline: 14 7 2022
entrez: 14 5 2022
Statut: ppublish

Résumé

Cerebral 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. We 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. SCG 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. SCG 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). In 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.

Identifiants

pubmed: 35567916
pii: S1566-0702(22)00046-7
doi: 10.1016/j.autneu.2022.102987
pmc: PMC9659432
mid: NIHMS1843296
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

102987

Subventions

Organisme : NINDS NIH HHS
ID : R25 NS079198
Pays : United States

Informations de copyright

Copyright © 2022 Elsevier B.V. All rights reserved.

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Auteurs

Wi Jin Kim (WJ)

Department of Neurosurgery, University of California Los Angeles, Los Angeles, CA, USA.

Michael Dacey (M)

Cardiac Arrhythmia Center, Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA.

Hashitha Milan Samarage (HM)

Department of Neurosurgery, University of California Los Angeles, Los Angeles, CA, USA.

David Zarrin (D)

David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.

Keshav Goel (K)

David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.

Christopher Chan (C)

Cardiac Arrhythmia Center, Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA.

Xin Qi (X)

David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.

Anthony C Wang (AC)

Department of Neurosurgery, University of California Los Angeles, Los Angeles, CA, USA.

Kalyanam Shivkumar (K)

Cardiac Arrhythmia Center, Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA.

Jeffrey Ardell (J)

Cardiac Arrhythmia Center, Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA.

Geoffrey P Colby (GP)

Department of Neurosurgery, University of California Los Angeles, Los Angeles, CA, USA. Electronic address: gcolby@mednet.ucla.edu.

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Classifications MeSH