| Enhanced vulnerability to secondary ischemic insults after experimental traumatic brain injury. | |
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MedLine Citation:
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PMID: 7496745 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Both experimental traumatic brain injury and clinical traumatic brain injury appear to render the brain more vulnerable to a second ischemic insult. The mechanisms of enhanced vulnerability to subsequent ischemia appear to include a reduced ability to increase cerebral blood flow in response to hypotension, hypoxemia, or acute anemia and increased tissue sensitivity to ischemia. Although numerous mediators may be involved in increased tissue sensitivity, those that particularly merit investigation include oxygen free radicals, glutamate, arachidonate metabolites, calcium ions, and protein kinase C. |
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Authors:
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D S DeWitt; L W Jenkins; D S Prough |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S.; Review |
Journal Detail:
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Title: New horizons (Baltimore, Md.) Volume: 3 ISSN: 1063-7389 ISO Abbreviation: New Horiz Publication Date: 1995 Aug |
Date Detail:
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Created Date: 1996-01-16 Completed Date: 1996-01-16 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 9416195 Medline TA: New Horiz Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 376-83 Citation Subset: IM |
Affiliation:
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Department of Anesthesiology, University of Texas Medical Branch, Galveston 77555-0591, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Brain Injuries / complications* Brain Ischemia / etiology, metabolism, physiopathology* Cats Cerebrovascular Circulation Disease Susceptibility / physiopathology Humans Hypoxia, Brain / etiology, metabolism, physiopathology Rats |
| Grant Support | |
ID/Acronym/Agency:
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NS19355/NS/NINDS NIH HHS; NS19550/NS/NINDS NIH HHS |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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