Endothelial nitric oxide synthase pathophysiology after nonocclusive common carotid artery thrombosis in rats

Gary H. Danton, Ricardo Prado, Jessie Truettner, Brant D. Watson, W. Dalton Dietrich

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)612-619
Number of pages8
JournalJournal of Cerebral Blood Flow and Metabolism
Volume22
Issue number5
DOIs
StatePublished - 2002

Keywords

  • Cerebral arteries
  • Cerebrovascular accident
  • Cranial window
  • Endothelial constitutive nitric oxide synthase
  • Rat
  • Thromboembolism

ASJC Scopus subject areas

  • Endocrinology
  • Neuroscience(all)
  • Endocrinology, Diabetes and Metabolism

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