NK1 tachykinin receptor antagonist treatment reduces cerebral edema and intracranial pressure in an ovine model of ischemic stroke.

Cerebral edema NK1-R intracranial pressure stroke translation

Journal

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
ISSN: 1559-7016
Titre abrégé: J Cereb Blood Flow Metab
Pays: United States
ID NLM: 8112566

Informations de publication

Date de publication:
28 Mar 2024
Historique:
medline: 28 3 2024
pubmed: 28 3 2024
entrez: 28 3 2024
Statut: aheadofprint

Résumé

Following ischemic stroke, substance P (SP)-mediated neurogenic inflammation is associated with profound blood-brain barrier (BBB) dysfunction, cerebral edema, and elevated intracranial pressure (ICP). SP elicits its effects by binding the neurokinin 1 tachykinin receptor (NK1-R), with administration of an NK1-R antagonist shown to ameliorate BBB dysfunction and cerebral edema in rodent and permanent ovine stroke models. Given the importance of reperfusion in clinical stroke, this study examined the efficacy of NK1-R antagonist treatment in reducing cerebral edema and ICP in an ovine model of transient middle cerebral artery occlusion (tMCAo). Anesthetized sheep (

Identifiants

pubmed: 38546535
doi: 10.1177/0271678X241241907
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

271678X241241907

Déclaration de conflit d'intérêts

Declaration of conflicting interestsThe author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: The NK1-R antagonist drug (EU-C-001) was kindly donated by PresSura Neuro, however, they had no input in the experimental design, conduct of the study, nor data analysis.

Auteurs

Annabel J Sorby-Adams (AJ)

School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia.

Oana C Marian (OC)

School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia.

Isabella M Bilecki (IM)

School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia.

Levi E Elms (LE)

School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia.

Nawaf Yassi (N)

Department of Medicine and Neurology, Melbourne Brain Centre at the Royal Melbourne Hospital, University of Melbourne, Parkville, Victoria, Australia.
Population Health and Immunity Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.

Rebecca J Hood (RJ)

School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia.

Janet K Coller (JK)

School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia.

Shannon M Stuckey (SM)

School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia.

W Taylor Kimberly (WT)

Department of Neurology and the Center for Genomic Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.

Tracy D Farr (TD)

School of Life Sciences, University of Nottingham, Nottingham, UK.

Anna V Leonard (AV)

School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia.

Emma Thornton (E)

School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia.

Robert Vink (R)

Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia.

Renée J Turner (RJ)

School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia.

Classifications MeSH