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dc.contributor.authorErgul, Adviye
dc.contributor.authorElgebaly, Mostafa M
dc.contributor.authorMiddlemore, Mary-Louise
dc.contributor.authorLi, Weiguo
dc.contributor.authorElewa, Hazem
dc.contributor.authorSwitzer, Jeffrey A
dc.contributor.authorHall, Christiana
dc.contributor.authorKozak, Anna
dc.contributor.authorFagan, Susan C
dc.date.accessioned2013-06-12T14:40:20Z
dc.date.available2013-06-12T14:40:20Z
dc.date.issued2007-10-15
dc.identifier.citationBMC Neurology. 2007 Oct 15;7(1):33
dc.identifier.urihttp://dx.doi.org/10.1186/1471-2377-7-33
dc.identifier.urihttp://hdl.handle.net/10724/19530
dc.description.abstractAbstract Background Interruption of flow through of cerebral blood vessels results in acute ischemic stroke. Subsequent breakdown of the blood brain barrier increases cerebral injury by the development of vasogenic edema and secondary hemorrhage known as hemorrhagic transformation (HT). Diabetes is a risk factor for stroke as well as poor outcome of stroke. The current study tested the hypothesis that diabetes-induced changes in the cerebral vasculature increase the risk of HT and augment ischemic injury. Methods Diabetic Goto-Kakizaki (GK) or control rats underwent 3 hours of middle cerebral artery occlusion and 21 h reperfusion followed by evaluation of infarct size, hemorrhage and neurological outcome. Results Infarct size was significantly smaller in GK rats (10 ± 2 vs 30 ± 4%, p < 0.001). There was significantly more frequent hematoma formation in the ischemic hemisphere in GK rats as opposed to controls. Cerebrovascular tortuosity index was increased in the GK model (1.13 ± 0.01 vs 1.34 ± 0.06, P < 0.001) indicative of changes in vessel architecture. Conclusion These findings provide evidence that there is cerebrovascular remodeling in diabetes. While diabetes-induced remodeling appears to prevent infarct expansion, these changes in blood vessels increase the risk for HT possibly exacerbating neurovascular damage due to cerebral ischemia/reperfusion in diabetes.
dc.titleIncreased hemorrhagic transformation and altered infarct size and localization after experimental stroke in a rat model of type 2 diabetes
dc.typeJournal Article
dc.date.updated2013-06-07T19:04:19Z
dc.description.versionPeer Reviewed
dc.language.rfc3066en
dc.rights.holderAdviye Ergul et al.; licensee BioMed Central Ltd.


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