Research article

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

Adviye Ergul^1,2 , Mostafa M Elgebaly¹ , Mary-Louise Middlemore¹ , Weiguo Li¹ , Hazem Elewa¹ , Jeffrey A Switzer³ , Christiana Hall³ , Anna Kozak^1,4 and Susan C Fagan^1,3,4

¹Program in Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, USA

²Vascular Biology Center, Medical College of Georgia, USA

³Department of Neurology, Medical College of Georgia, USA

⁴Specialty Care Service Line, Veterans, Administration Medical Center, Augusta, GA, USA

author email corresponding author email

BMC Neurology 2007, 7:33doi:10.1186/1471-2377-7-33

Published:	15 October 2007

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.