Neurovascular protection by ischemic tolerance: role of nitric oxide and reactive oxygen species.

Neurovascular protection by ischemic tolerance: role of nitric oxide and reactive oxygen species. Research Abstract Details 

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Neurovascular protection by ischemic tolerance: role of nitric oxide and reactive oxygen species. Abstract Text:

Alexander Kunz,Laibaik Park,Takato Abe,Eduardo F Gallo,Josef Anrather,Ping Zhou,Costantino Iadecola,

Cerebral ischemic preconditioning or tolerance is a powerful neuroprotective phenomenon by which a sublethal injurious stimulus renders the brain resistant to a subsequent damaging ischemic insult. We used lipopolysaccharide (LPS) as a preconditioning stimulus in a mouse model of middle cerebral artery occlusion (MCAO) to examine whether improvements in cerebrovascular function contribute to the protective effect. Administration of LPS 24 h before MCAO reduced the infarct by 68% and improved ischemic cerebral blood flow (CBF) by 114% in brain areas spared from infarction. In addition, LPS prevented the dysfunction in cerebrovascular regulation induced by MCAO, as demonstrated by normalization of the increase in CBF produced by neural activity, hypercapnia, or by the endothelium-dependent vasodilator acetylcholine. These beneficial effects of LPS were not observed in mice lacking inducible nitric oxide synthase (iNOS) or the nox2 subunit of the superoxide-producing enzyme NADPH oxidase. LPS increased reactive oxygen species and the peroxynitrite marker 3-nitrotyrosine in wild-type mice but not in nox2 nulls. The peroxynitrite decomposition catalyst 5,10,15,20-tetrakis(4-sulfonatophenyl)porphyrinato iron (III) attenuated LPS-induced nitration and counteracted the beneficial effects of LPS on infarct volume, ischemic CBF, and vascular reactivity. Thus, LPS preserves neurovascular function and ameliorates CBF in regions of the ischemic territory at risk for infarction. This effect is mediated by peroxynitrite formed from iNOS-derived NO and nox2-derived superoxide. The data indicate that preservation of cerebrovascular function is an essential component of ischemic tolerance and suggest that combining neuroprotection and vasoprotection may be a valuable strategy for treating ischemic brain injury.

Neurovascular protection by ischemic tolerance: role of nitric oxide and reactive oxygen species. Publishing Authors By Initials

A Kunz,L Park,T Abe,EF Gallo,J Anrather,P Zhou,C Iadecola,

For similar inorganic chemicals: free radicals: reactive oxygen species research abstracts see: inorganic chemicals: free radicals: reactive oxygen species research

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MEDLINE DATE:

Neurovascular protection by ischemic tolerance: role of nitric oxide and reactive oxygen species. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of neuroscience : the official journal

VOLUME: 27

Page Numbers: 7083-93

Journal Abbreviation: J. Neurosci.

ISSN: 1529-2401

DAY: 4

MONTH: Jul

YEAR: 2007

Neurovascular protection by ischemic tolerance: role of nitric oxide and reactive oxygen species. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8102140

Neurovascular protection by ischemic tolerance: role of nitric oxide and reactive oxygen species. Keywords Mesh Terms:

KEYWORDS: Reactive Oxygen Species

MESH TERMS: metabolism

Chemical & Substance for Abstract: Neurovascular protection by ischemic tolerance: role of nitric oxide and reactive oxygen species. Information

Substance Name: Nitric Oxide Synthase Type II

Registry Number: EC 1.14.13.39

Grant and Affiliation Information for Neurovascular protection by ischemic tolerance: role of nitric oxide and reactive oxygen species.

AFFILIATION: Division of Neurobiology, Weill-Cornell Medical College, KB-410, New York, New York 10021, USA.

Country: United States

AGENCY: United States NINDS

GRANT: NS35806

ACRONYM: NS

MEDLINETA: J Neurosci

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