Document Detail


Endothelial nitric oxide synthase pathophysiology after nonocclusive common carotid artery thrombosis in rats.
MedLine Citation:
PMID:  11973434     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although vascular dysregulation has been documented in patients with extracranial vascular disease, transient ischemic attacks, and stroke, the pathomechanisms are poorly understood. To model thromboembolic stroke in rats, photochemically induced nonocclusive common carotid artery thrombosis (CCAT) was used to generate a platelet thrombus in the carotid artery of anesthetized rats. After CCAT, platelet aggregates break off the thrombus, travel to the distal cerebral vasculature, damage blood vessels, and cause small infarctions. The authors hypothesized that deficits in the endothelial nitric oxide synthase (eNOS) pathway may be responsible for vascular dysfunction after embolic stroke. To examine the functional status of the eNOS system, they measured eNOS-dependent dilation after CCAT by applying acetylcholine through a cranial window over the middle cerebral artery. The authors also measured eNOS mRNA and protein in the middle cerebral artery to determine whether functional changes were caused by alterations in expression. eNOS-dependent dilation was reduced at 6 hours, elevated at 24 hours, and returned to baseline 72 hours after CCAT. Endothelial nitric oxide synthase mRNA increased at 2 hours and was followed by a rise in protein 24 hours after CCAT. Changes in the eNOS system may account for some of the observed vascular deficits in patients with cerebrovascular disease.
Authors:
Gary H Danton; Ricardo Prado; Jessie Truettner; Brant D Watson; W Dalton Dietrich
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism     Volume:  22     ISSN:  0271-678X     ISO Abbreviation:  J. Cereb. Blood Flow Metab.     Publication Date:  2002 May 
Date Detail:
Created Date:  2002-04-25     Completed Date:  2002-06-04     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8112566     Medline TA:  J Cereb Blood Flow Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  612-9     Citation Subset:  IM    
Affiliation:
Department of Neurological Surgery, University of Miami School of Medicine, Miami, FL 33101, U.S.A.
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / pharmacology
Animals
Blotting, Western
Carotid Artery Thrombosis / enzymology*,  physiopathology
Carotid Artery, Common*
Disease Models, Animal
Endothelium, Vascular / physiopathology
Gene Expression
Kinetics
Male
Middle Cerebral Artery / drug effects,  enzymology,  physiopathology
Nitric Oxide Synthase / genetics,  physiology*
Nitric Oxide Synthase Type III
Photochemistry
Platelet Aggregation
RNA, Messenger / analysis
Rats
Rats, Wistar
Reverse Transcriptase Polymerase Chain Reaction
Stroke / enzymology,  physiopathology
Vasodilation / drug effects
Grant Support
ID/Acronym/Agency:
NS 07459-01/NS/NINDS NIH HHS; NS 23244-16/NS/NINDS NIH HHS; NS 27127-11/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/RNA, Messenger; 51-84-3/Acetylcholine; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, rat

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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