Left Carotid Artery Thrombosis Due to Thromboangiitis Obliterans

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Melanie E. Bourgeau ◽  
Phillip G. Key ◽  
Jesse Chou ◽  
Joseph A. Prahlow
Keyword(s):  
Carotid Artery ◽  
Thromboangiitis Obliterans ◽  
Left Carotid Artery ◽  
Carotid Artery Thrombosis ◽  
Artery Thrombosis

scholarly journals Ferric Chloride-induced Canine Carotid Artery Thrombosis: A Large Animal Model of Vascular Injury

10.3791/57981 ◽  
2018 ◽  
Author(s):  
Allyson L. Huttinger ◽  
Debra G. Wheeler ◽  
Surya Gnyawali ◽  
David Dornbos ◽  
Juliana M. Layzer ◽  
...  
Keyword(s):  
Animal Model ◽  
Carotid Artery ◽  
Vascular Injury ◽  
Ferric Chloride ◽  
Large Animal Model ◽  
Large Animal ◽  
Carotid Artery Thrombosis ◽  
Artery Thrombosis

INTERNAL CAROTID ARTERY THROMBOSIS FOLLOWING SOFT PALATE INJURIES

1984 ◽  
Vol 94 (12) ◽  
pp. 1571???1575 ◽  
Author(s):  
ARTHUR S. HENGERER ◽  
TERRY R. DEGROOT ◽  
ROBERT J. RIVERS ◽  
DANIEL S. PETTEE
Keyword(s):  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Soft Palate ◽  
Internal Carotid ◽  
Carotid Artery Thrombosis ◽  
Artery Thrombosis

scholarly journals Endothelial Nitric Oxide Synthase Pathophysiology after Nonocclusive Common Carotid Artery Thrombosis in Rats

2002 ◽  
Vol 22 (5) ◽  
pp. 612-619 ◽  
Author(s):  
Gary H. Danton ◽  
Ricardo Prado ◽  
Jessie Truettner ◽  
Brant D. Watson ◽  
W. Dalton Dietrich
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Carotid Artery ◽  
Middle Cerebral Artery ◽  
Common Carotid Artery ◽  
Endothelial Nitric Oxide Synthase ◽  
Carotid Artery Thrombosis ◽  
Artery Thrombosis ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

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.

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