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目的观察兔大脑中动脉阻塞后常规MRI及DWI表现,阐明活体脑缺血后DWI的演变规律及其病理生理机制方法40只成年新西兰大白兔随机分成2组,对照组4只,实验组36只实验组采用Yamamoto法制作急性大脑中动脉阻塞(MCAO)模型,对照组仅曝露大脑中动脉,而不结扎观察MCAO后缺血区在各时段ADC值的变化规律,并进行病理学检查结果对照组:T2WI及DWI均无高信号出现,光镜检查均无异常改变实验组:DWI上,MCAO后0.5h基底节区出现高信号;T2WI最早于2h出现高信号,早期ADC值快速下降的病理基础是缺血后细胞内的水含量的增加;ADC值下降减慢及相对平台期的病理基础是血脑屏障破坏的逐渐加重及血管源性水肿的出现;而ADC值的上升的病理基础是细胞的死亡、溶解,血脑屏障的破坏结论早期的扩散异常区域并不意味着病灶已发生梗死,当持续缺血达6h以上,脑组织将产生不可逆的损伤
Objective To observe the manifestations of conventional MRI and DWI after occlusion of middle cerebral artery (MCA) in rabbits, and to clarify the evolvement of DWI and the pathophysiological mechanism after living cerebral ischemia.Methods Forty adult New Zealand white rabbits were randomly divided into two groups: control group (n = 36), experimental group In the experimental group, the model of middle cerebral artery occlusion (MCAO) was made by Yamamoto method, the middle cerebral artery was exposed only in the control group, and the change of ADC value of the ischemic area at various time after MCAO was observed without ligation. The pathological examination results of control group : There was no high signal on both T2WI and DWI, and there was no abnormal change on light microscope. Experimental group: high signal appeared in basal ganglia of 0.5h on DWI and MCAO; the pathological basis of high signal on T2WI and early rapid ADC value decreased on T2WI Is the increase of intracellular water content after ischemia; the decrease of ADC value and the pathological basis of relative plateau phase are the gradual increase of blood-brain barrier disruption and the appearance of vasogenic edema; and the pathological basis of ADC value rise is the cell Of the death, dissolution, the destruction of the blood-brain barrier conclusion of the early proliferation of anomalous areas does not mean that the lesion has occurred infarction, when the sustained ischemia up to 6h, brain tissue will have irreversible damage