title: Mechanism of the sex difference in endothelial dysfunction after stroke.
abstract: Stroke, the number four cause of death in the United States, is a greatly debilitating event resulting from insufficient blood supply to the brain (cerebral ischemia). Endothelial dysfunction, primarily characterized by dampened endothelial- dependent vasodilation, is a major contributor to the development and outcome of stroke. This review discusses the role of soluble epoxide hydrolase (sEH), an enzyme responsible for the degradation of vasoprotective eicosatrienoic acids (EETs), in the context of the cerebral vasculature and its contribution to the sexual dimorphic nature of stroke.
authors.affiliation: Cerebrovascular Research Division, Department of Anesthesiology & Perioperative Medicine, Oregon Health & Science University, Portland, OR 97239-3098, USA.
authors.forename: Catherine M
authors.initials: CM
authors.lastname: Davis
authors.forename: Stacy L
authors.initials: SL
authors.lastname: Fairbanks
authors.forename: Nabil J
authors.initials: NJ
authors.lastname: Alkayed
mesh_terms: D000818:Animals; D001095:Arachidonic Acids / Q000502:physiology; D002545:Brain Ischemia / Q000188:drug therapy / Q000503:physiopathology; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000503:physiopathology*; D004851:Epoxide Hydrolases / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000502:physiology; D005849:Gerbillinae; D006801:Humans; D008297:Male; D051379:Mice; D018696:Neuroprotective Agents / Q000494:pharmacology; D051381:Rats; D012727:Sex Characteristics; D020521:Stroke / Q000188:drug therapy / Q000503:physiopathology*
chemical_list: D001095:Arachidonic Acids; D018696:Neuroprotective Agents; D004851:Epoxide Hydrolases
keywords: EET; brain; endothelia; ischemia; sEH; sexual dimorphism