Hypoxia-related mechanisms inducing acute mountain sickness and migraine.
AMS
CGRP
HAH
human migraine model
hypoxia
migraine
Journal
Frontiers in physiology
ISSN: 1664-042X
Titre abrégé: Front Physiol
Pays: Switzerland
ID NLM: 101549006
Informations de publication
Date de publication:
2022
2022
Historique:
received:
14
07
2022
accepted:
15
08
2022
entrez:
23
9
2022
pubmed:
24
9
2022
medline:
24
9
2022
Statut:
epublish
Résumé
Experimental models of human diseases are vital for pathophysiological and therapeutic research. To investigate the initiation, maintenance, pathophysiology and even termination of a migraine/headache attack these models are urgently needed. Results from different studies promote the profound involvement of hypoxia in migraine and other primary/secondary headaches. The possible mechanisms that drive the induction of headaches through hypoxia are still unknown, but several modes of action, such as increased blood flow, dilation of cerebral arteries, the release of nitroglycerin, calcitonin gene-related peptide and adenosine or increased oxygen extraction are discussed intensively. In studies exposing healthy volunteers and people with a history of migraine to controlled normobaric hypoxia, our research group could demonstrate normobaric hypoxia to be an effective trigger of migraine headaches. Furthermore, a longitudinal measurement of calcitonin gene-related peptide (CGRP), during a hypoxic challenge in migraine patients, revealed increasing CGRP levels with prolonged hypoxic challenge. Since GRP has been linked to migraine and other headache disorders, hypoxia could be regarded as initiator for headaches on a neurotransmitter basis. Furthermore, it has been known for more than 2 decades from studies
Identifiants
pubmed: 36148300
doi: 10.3389/fphys.2022.994469
pii: 994469
pmc: PMC9485719
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
994469Informations de copyright
Copyright © 2022 Frank, Kaltseis, Filippi and Broessner.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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