Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2002-4-25
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0271-678X
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
612-9
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11973434-Acetylcholine, pubmed-meshheading:11973434-Animals, pubmed-meshheading:11973434-Blotting, Western, pubmed-meshheading:11973434-Carotid Artery, Common, pubmed-meshheading:11973434-Carotid Artery Thrombosis, pubmed-meshheading:11973434-Disease Models, Animal, pubmed-meshheading:11973434-Endothelium, Vascular, pubmed-meshheading:11973434-Gene Expression, pubmed-meshheading:11973434-Kinetics, pubmed-meshheading:11973434-Male, pubmed-meshheading:11973434-Middle Cerebral Artery, pubmed-meshheading:11973434-Nitric Oxide Synthase, pubmed-meshheading:11973434-Nitric Oxide Synthase Type III, pubmed-meshheading:11973434-Photochemistry, pubmed-meshheading:11973434-Platelet Aggregation, pubmed-meshheading:11973434-RNA, Messenger, pubmed-meshheading:11973434-Rats, pubmed-meshheading:11973434-Rats, Wistar, pubmed-meshheading:11973434-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:11973434-Stroke, pubmed-meshheading:11973434-Vasodilation
pubmed:year
2002
pubmed:articleTitle
Endothelial nitric oxide synthase pathophysiology after nonocclusive common carotid artery thrombosis in rats.
pubmed:affiliation
Department of Neurological Surgery, University of Miami School of Medicine, Miami, FL 33101, U.S.A.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't