Increased hemorrhagic transformation and altered infarct size and localization after experimental stroke in a rat model type 2 diabetes.
Increased hemorrhagic transformation and altered infarct size and localization after experimental stroke in a rat model type 2 diabetes.
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DOI：
10.1186/1471-2377-7-33
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发表时间：
2007-10-15
期刊：
影响因子：
2.6
通讯作者：
Fagan, Susan C.
中科院分区：
文献类型：
--
作者：
Ergul, Adviye;Elgebaly, Mostafa M.;Middlemore, Mary-Louise;Li, Weiguo;Elewa, Hazem;Switzer, Jeffrey A.;Hall, Christiana;Kozak, Anna;Fagan, Susan C.
脑血管流通的中断导致急性缺血性中风。血脑屏障的随后破坏通过血管源性水肿和称为出血性转化（HT）的继发性出血的发展而增加脑损伤。糖尿病是中风的危险因素，也是中风预后不良的因素。目前的研究验证了糖尿病引起的脑血管变化增加HT风险和增加缺血性损伤的假设。糖尿病Goto-Kakizaki（GK）或对照组大鼠进行3小时的大脑中动脉闭塞和21小时的再灌注，然后评估梗死面积，出血和神经功能的结果。GK大鼠的脑体积显著较小（10 ± 2 vs 30 ± 4%，p < 0.001）。与对照组相比，GK大鼠缺血半球的血肿形成频率明显更高。脑血管迂曲指数在GK模型中增加（1.13 ± 0.01 vs 1.34 ± 0.06，P < 0.001），提示血管结构的改变。这些发现为糖尿病患者存在脑血管重构提供了证据。虽然糖尿病诱导的重塑似乎可以防止梗死扩大，但血管的这些变化增加了HT的风险，可能加剧糖尿病脑缺血/再灌注引起的神经血管损伤。
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. 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. 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. 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.
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