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Molecular biological considerations in cerebral vasospasm following aneurysmal subarachnoid hemorrhage.
MedLine Citation:
PMID:  15104415     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Chronic delayed cerebral vasospasm (CDCV) remains a serious and often fatal complication of aneurysmal subarachnoid hemorrhage (SAH). The current understanding of its fundamental mechanisms and molecular biological characterization is rudimentary. Two important vasoactive substances have been implicated in CDCV: endothelin-1 (ET-1) and nitric oxide (NO). A 21--amino acid vasoconstrictor peptide, ET-1 has generated interest as a possible important contributor to cerebral vasospasm on the basis of both clinical and experimental evidence suggesting abnormally enhanced production. Nitric oxide is a cell membrane--permeable free radical gas that accounts for the vasodilatory effect of endothelium-derived relaxation factor and is a physiological antagonist of ET-1. As with ET-1, abnormalities of NO production have been implicated in several pathological conditions including cerebral vasospasm. This brief report reviews some of the physiological and regulatory features of these two molecules and explores the possibility of their relationship to cerebral vasospasm.
J E Thomas
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Neurosurgical focus     Volume:  3     ISSN:  1092-0684     ISO Abbreviation:  Neurosurg Focus     Publication Date:  1997 Sep 
Date Detail:
Created Date:  2004-04-23     Completed Date:  2004-05-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100896471     Medline TA:  Neurosurg Focus     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e3     Citation Subset:  -    
Department of Neurological Surgery, Thomas Jefferson University and Wills Neurosensory Institute, Philadelphia, Pennsylvania 19107, USA.
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