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dc.contributor.authorGursoy-Ozdemir, Y
dc.contributor.authorCan, A
dc.contributor.authorDalkara, T
dc.date.accessioned2019-12-10T11:25:54Z
dc.date.available2019-12-10T11:25:54Z
dc.date.issued2004
dc.identifier.issn0039-2499
dc.identifier.urihttps://doi.org/10.1161/01.STR.0000126044.83777.f4
dc.identifier.urihttp://hdl.handle.net/11655/15731
dc.description.abstractBackground and Purpose-Use of thrombolysis in stroke is limited by a short therapeutic window because delayed reperfusion may cause brain hemorrhage and edema. Available evidence suggests a role for superoxide, NO, and peroxynitrite in reperfusion-induced injury. However, depending on their cellular origin and interactions between them, these molecules may exert protective or deleterious actions, neither of which is characterized in the intact brain. Methods-Using fluorescent probes, we determined superoxide and peroxynitrite formation within neurons, astrocytes, and endothelium, and the association between oxidative/nitrative stress and vascular injury in mice brains subjected to 2-hour middle cerebral artery occlusion and 3 or 5 hours of reperfusion. Results-Both signals were colocalized, suggesting that the main source of peroxynitrite in the reperfused brain was a reaction between superoxide and NO. Superoxide and peroxynitrite formation was particularly intense in microvessels and astrocytic end-feet surrounding them, and overlapped with dense mitochondrial labeling. Sites of oxidative/nitrative stress on microvessels were colocalized with markers of vascular injury such as Evans blue (EB) leakage and matrix metalloproteinase-9 (MMP-9) expression, suggesting an association between peroxynitrite and microvascular injury. Supporting this idea, partial inhibition of endothelial NO synthesis at reperfusion with a low dose of L-nitroarginine (1 mg/kg IP) reduced 3-nitrotyrosine formation in microvessels and EB extravasation. Conclusion-During reperfusion, intense superoxide, NO, and peroxynitrite formation on microvessels and surrounding end-feet may lead to cerebral hemorrhage and edema by disrupting microvascular integrity. Combination of thrombolysis with agents diminishing oxidative/nitrative stress may reduce reperfusion-induced injury and extend the therapeutic window for thrombolysis.
dc.language.isoen
dc.publisherLippincott Williams & Wilkins
dc.relation.isversionof10.1161/01.STR.0000126044.83777.f4
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectNeurosciences & Neurology
dc.subjectCardiovascular System & Cardiology
dc.titleReperfusion-Induced Oxidative/Nitrative Injury To Neurovascular Unit After Focal Cerebral Ischemia
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.relation.journalStroke
dc.contributor.departmentNöroloji
dc.identifier.volume35
dc.identifier.issue6
dc.identifier.startpage1449
dc.identifier.endpage1453
dc.description.indexWoS
dc.description.indexScopus


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