Persistent Cerebrovascular Damage After Stroke in Type Two Diabetic Rats Measured by Magnetic Resonance Imaging

Background and Purpose-Diabetes mellitus is a disease with vascular components. Consequently, the blood-brain barrier disruption after stroke may differ between diabetic and nondiabetic animals. However, few studies have documented the longitudinal blood-brain barrier disruption afte stroke in diabetic animals. In this study, using MRI, we noninvasively evaluated the blood-brain barrier damage after middle cerebral artery occlusion in diabetic and nondiabetic rats. Methods-Type 2 diabetes mellitus (T2DM) was induced in adult male Wistar rats by administration of a high-fat diet in combination with a single intraperitoneal injection (35 mg/kg) of streptozotocin. T2DM rats (n=9) and nondiabetic wildtype (WT) rats (n=9) were subjected to middle cerebral artery occlusion for 2 hours using the filament model. MRI was performed 1 day and then weekly for 5 weeks after middle cerebral artery occlusion for all rats. Results-The ischemic lesion volumes after stroke as measured using T-2 maps were not significantly different between the T2DM and WT rats. Compared with the WT rats, the volumes of blood-brain barrier disruption evaluated using contrast-enhanced T-1-weighted imaging with gadolinium-diethylenetriamine penta-acetic acid and the cerebral hemorrhagic volumes measured with susceptibility-weighted imaging were significantly (P<0.05) larger in the T2DM rats from 1 to 5 weeks after stroke; values of diffusion fractional anisotropy were significantly lower in T2DM rats (P<0.03) than in WT rats after stroke. These MRI measurements were consistent with histological data. Conclusions-Using MRI, T-2-weighted imaging did not detect significant differences of the ischemic lesion volumes between T2DM and WT rats. In contrast to the WT rats, however, contrast-enhanced T 1 -weighted imaging and susceptibility-weighted imaging identified much more severe ischemic vascular damage, whereas fractional anisotropy demonstrated lower axonal density in the T2DM rats after stroke.