Pathogenesis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage: putative mechanisms and novel approaches
Pathogenesis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage: putative mechanisms and novel approaches
Cerebral vasospasm is a potentially incapacitating or lethal complication in patients with aneurysmal subarachnoid hemorrhage (SAH). The development of effective preventative and therapeutic interventions has been largely hindered by the fact that the underlying pathogenic mechanisms of cerebral vasospasm remain poorly understood. However, intensive research during the last 3 decades has identified certain mechanisms that possibly play a role in its development. Experimental data suggest that calcium-dependent and -independent vasoconstriction is taking place during vasospasm. It appears that the breakdown products of blood in the subarachnoid space are involved, through direct and/or indirect pathways, in the development of vasospasm after SAH. Free radicals reactions, an imbalance between vasoconstrictor and vasodilator substances (endothelium derived substances, e.g., nitric oxide, endothelin; arachidonic acid metabolites, e.g., prostaglandins, prostacyclin), inflammatory processes, an upheaval of neuronal mechanisms that regulate vascular tone, endothelial proliferation, and apoptosis have all been put forward as causative and/or pathogenic factors. Translational research in the field of vasospasm has traditionally aimed to identify agents/interventions in order to block the cascades initiated after SAH. The combination of novel approaches such as cerebral microdialysis, magnetic resonance spectroscopy, proteomics, and lipidomics could serve a dual purpose: elucidating the complex pathobiochemistry of vasospasm and providing clinicians with tools for early detection of this feared complication. The purpose of this Mini-Review is to provide an overview of the pathogenesis of cerebral vasospasm and of novel approaches used in basic and translational research.
stroke, cerebral aneurysm, delayed ischaemic neurological deficit, vasoconstriction, smooth muscle contraction, microdialysis
1-11
Kolias, Angelos G.
aef2742e-e557-43a3-9d48-1a269bc5814e
Sen, Jon
464edd7f-7891-4e3f-a86c-0675fd129828
Belli, Antonio
33707b7b-b004-4245-aead-98a8e1e2b2e2
January 2009
Kolias, Angelos G.
aef2742e-e557-43a3-9d48-1a269bc5814e
Sen, Jon
464edd7f-7891-4e3f-a86c-0675fd129828
Belli, Antonio
33707b7b-b004-4245-aead-98a8e1e2b2e2
Kolias, Angelos G., Sen, Jon and Belli, Antonio
(2009)
Pathogenesis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage: putative mechanisms and novel approaches.
Journal of Neuroscience Research, 87 (1), .
(doi:10.1002/jnr.21823).
(PMID:18709660)
Abstract
Cerebral vasospasm is a potentially incapacitating or lethal complication in patients with aneurysmal subarachnoid hemorrhage (SAH). The development of effective preventative and therapeutic interventions has been largely hindered by the fact that the underlying pathogenic mechanisms of cerebral vasospasm remain poorly understood. However, intensive research during the last 3 decades has identified certain mechanisms that possibly play a role in its development. Experimental data suggest that calcium-dependent and -independent vasoconstriction is taking place during vasospasm. It appears that the breakdown products of blood in the subarachnoid space are involved, through direct and/or indirect pathways, in the development of vasospasm after SAH. Free radicals reactions, an imbalance between vasoconstrictor and vasodilator substances (endothelium derived substances, e.g., nitric oxide, endothelin; arachidonic acid metabolites, e.g., prostaglandins, prostacyclin), inflammatory processes, an upheaval of neuronal mechanisms that regulate vascular tone, endothelial proliferation, and apoptosis have all been put forward as causative and/or pathogenic factors. Translational research in the field of vasospasm has traditionally aimed to identify agents/interventions in order to block the cascades initiated after SAH. The combination of novel approaches such as cerebral microdialysis, magnetic resonance spectroscopy, proteomics, and lipidomics could serve a dual purpose: elucidating the complex pathobiochemistry of vasospasm and providing clinicians with tools for early detection of this feared complication. The purpose of this Mini-Review is to provide an overview of the pathogenesis of cerebral vasospasm and of novel approaches used in basic and translational research.
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e-pub ahead of print date: 15 August 2008
Published date: January 2009
Keywords:
stroke, cerebral aneurysm, delayed ischaemic neurological deficit, vasoconstriction, smooth muscle contraction, microdialysis
Identifiers
Local EPrints ID: 142003
URI: http://eprints.soton.ac.uk/id/eprint/142003
ISSN: 0360-4012
PURE UUID: 4e83bb64-a54b-473f-b53d-4421509ef715
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Date deposited: 30 Mar 2010 11:30
Last modified: 14 Mar 2024 00:38
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Author:
Angelos G. Kolias
Author:
Jon Sen
Author:
Antonio Belli
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