Increased hemorrhagic transformation and altered infarct size and localization after experimental stroke in a rat model type 2 diabetes.

Hdl Handle:
http://hdl.handle.net/10675.2/74
Title:
Increased hemorrhagic transformation and altered infarct size and localization after experimental stroke in a rat model type 2 diabetes.
Authors:
Ergul, Adviye; Elgebaly, Mostafa M; Middlemore, Mary-Louise; Li, Weiguo; Elewa, Hazem; Switzer, Jeffrey A; Hall, Christiana; Kozak, Anna; Fagan, Susan C.
Abstract:
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.
Citation:
BMC Neurol. 2007 Oct 15; 7:33
Issue Date:
29-Nov-2007
URI:
http://hdl.handle.net/10675.2/74
DOI:
10.1186/1471-2377-7-33
PubMed ID:
17937795
PubMed Central ID:
PMC2098774
Type:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
ISSN:
1471-2377
Appears in Collections:
Vascular Biology Center: Faculty Research and Publication

Full metadata record

DC FieldValue Language
dc.contributor.authorErgul, Adviyeen_US
dc.contributor.authorElgebaly, Mostafa Men_US
dc.contributor.authorMiddlemore, Mary-Louiseen_US
dc.contributor.authorLi, Weiguoen_US
dc.contributor.authorElewa, Hazemen_US
dc.contributor.authorSwitzer, Jeffrey Aen_US
dc.contributor.authorHall, Christianaen_US
dc.contributor.authorKozak, Annaen_US
dc.contributor.authorFagan, Susan C.en_US
dc.date.accessioned2010-09-24T21:44:43Z-
dc.date.available2010-09-24T21:44:43Z-
dc.date.issued2007-11-29en_US
dc.identifier.citationBMC Neurol. 2007 Oct 15; 7:33en_US
dc.identifier.issn1471-2377en_US
dc.identifier.pmid17937795en_US
dc.identifier.doi10.1186/1471-2377-7-33en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/74-
dc.description.abstractBACKGROUND: 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.en_US
dc.rightsThe PMC Open Access Subset is a relatively small part of the total collection of articles in PMC. Articles in the PMC Open Access Subset are still protected by copyright, but are made available under a Creative Commons or similar license that generally allows more liberal redistribution and reuse than a traditional copyrighted work. Please refer to the license statement in each article for specific terms of use. The license terms are not identical for all articles in this subset.en_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Glucose / physiologyen_US
dc.subject.meshBrain Infarction / pathologyen_US
dc.subject.meshDiabetes Mellitus, Type 2 / pathology / physiopathologyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshInfarction, Middle Cerebral Artery / complications / pathologyen_US
dc.subject.meshIntracranial Hemorrhages / etiology / pathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMatrix Metalloproteinase 2 / metabolismen_US
dc.subject.meshNeurologic Examination / methodsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshReperfusionen_US
dc.subject.meshSeverity of Illness Indexen_US
dc.titleIncreased hemorrhagic transformation and altered infarct size and localization after experimental stroke in a rat model type 2 diabetes.en_US
dc.typeJournal Articleen_US
dc.typeResearch Support, N.I.H., Extramuralen_US
dc.typeResearch Support, Non-U.S. Gov'ten_US
dc.identifier.pmcidPMC2098774en_US
dc.contributor.corporatenameVascular Biology Centeren_US
dc.contributor.corporatenameDepartment of Neurologyen_US

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