Abstract

Diabetes worsens functional outcome after ischemic stroke and is associated with greater hemorrhagic transformation (HT) occurrence. We have shown that male diabetic Goto-Kakizaki (GK) rats develop greater HT and neurological deficit despite smaller infarcts after temporary (3/21 hr) middle cerebral artery occlusion (MCAO) induced by the suture model. The impact of the duration of ischemia/reperfusion (I/R) and the method of ischemia on neurovascular injury and functional outcome in diabetic stroke remain unknown. To address this gap, control Wistar and diabetic GK rats were subjected to 90 min/23 hr, 3 hr/21 hr, or 3 hr/7 day MCAO by suture occlusion or embolus placement. In all groups, infarct size, edema, HT occurrence and severity (hemoglobin level), and functional outcome (grip strength and composite deficit score) were measured (Table). Infarct size was smaller in GK rats with suture or embolic MCAO, but expanded with longer reperfusion period. Edema, HT occurrence and severity were all increased in GK rats after 90 min and 3 hr occlusion with the suture model, but not in the embolic MCAO. Motor deficit was greater in diabetic rats. These findings suggest that diabetes accelerates the development of HT and amplifies vascular damage especially in the suture model where blood flow is rapidly reestablished. These results highlight the importance of earlier vascular protection to improve neurological outcome of acute ischemic stroke in diabetes.

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