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目的探究2型糖尿病大鼠脑梗死后超急性期缺血半暗带(ischemic penumbra,IP)随时间变化趋势。材料与方法 2型糖尿病大鼠及血糖正常对照组大鼠各9只,制作永久性大脑中动脉闭塞(MCAO)模型,MCAO后30min、1 h、3 h、6 h、9 h、12 h分别行MR扩散加权成像(DWI)、扩散张量成像(DTI)及T2WI,测量并计算病灶核心区及边缘区的相对表观扩散系数(rADC)值,相对平均扩散系数(rDCavg)值、相对各向异性分数(rFA)值。结果 2型糖尿病大鼠脑缺血后3 h以内、血糖正常大鼠9 h以内,缺血边缘区与核心区之间rADC、rDCavg值差异存在统计学意义(P<0.05)。结论血糖正常大鼠脑IP存在的时间窗为9 h;2型糖尿病大鼠脑IP存在的时间窗<3 h。缺血前高血糖加速脑缺血后血管源性水肿的发展。
Objective To investigate the temporal changes of hyperacute ischemic penumbra (IP) in type 2 diabetic rats after cerebral infarction. MATERIALS AND METHODS Nine rats with type 2 diabetes mellitus and normal glucose control group were given a model of permanent middle cerebral artery occlusion (MCAO). After MCAO 30 min, 1 h, 3 h, 6 h, 9 h, 12 h MR diffusion weighted imaging (DWI), diffusion tensor imaging (DTI) and T2WI were performed to measure and calculate the relative apparent diffusion coefficient (rADC) value and relative diffusivity coefficient (rDCavg) An anisotropic fraction (rFA) value. Results There were significant differences in rADC and rDCavg between ischemic border and core within 3 hours after cerebral ischemia in type 2 diabetic rats and within 9 hours in normal blood glucose rats (P <0.05). Conclusion The time window of brain IP in rats with normal blood glucose is 9 h, and the time window of brain IP in type 2 diabetic rats is less than 3 h. Preischemic hyperglycemia accelerates the development of vasogenic edema after cerebral ischemia.