Endothelial nitric oxide synthase pathophysiology after nonocclusive common carotid artery thrombosis in rats. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism. [J Cereb Blood Flow Metab] Journal article

Title	Endothelial nitric oxide synthase pathophysiology after nonocclusive common carotid artery thrombosis in rats.
Author(s)	Danton GH, Prado R, Truettner J, Watson BD, Dietrich WD
Institution	Department of Neurological Surgery, University of Miami School of Medicine, Miami, FL 33101, U.S.A.
Source	J Cereb Blood Flow Metab 2002 May; 22(5):612-9.
MeSH	Acetylcholine Animals Blotting, Western Carotid Artery Thrombosis Carotid Artery, Common Cerebrovascular Accident Disease Models, Animal Endothelium, Vascular Gene Expression Kinetics Male Middle Cerebral Artery Nitric Oxide Synthase Nitric Oxide Synthase Type III Photochemistry Platelet Aggregation RNA, Messenger Rats Rats, Wistar Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Reverse Transcriptase Polymerase Chain Reaction Vasodilation
Abstract	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.
Language	eng
Pub Type(s)	Journal Article
PubMed ID	11973434

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