脑缺血后短T_1信号强度演变及其病理机制  

The progressive changes and the related pathological mechanism of high signal intensity on T_1WI after brain ischemia in rats

作　　者：任燕双[1] 张云亭[2] 刘松龄[2] 

机构地区：[1]中国中医研究院广安门医院CT室,北京100053 [2]天津医科大学总医院放射科,天津300052

出　　处：《中国临床医学影像杂志》2004年第2期61-65,共5页Journal of China Clinic Medical Imaging

摘　　要：目的:观察脑缺血后短T信号强度演变规律并揭示其病理机制。方法:将46只不同缺血-再通时间组的大1鼠模型,于不同时间点观察短T信号强度的演变,并行组织学检查。结果:短T信号以皮质区多见,并且出现时间早于基11底节区。短T信号强度在各MR检查时间点之间存在显著性差异(1F=3.746P<0.05,)。组织学检查可见出血、脂质沉积和蛋白质变性、髓鞘破坏等;皮质区短T信号主要与出血有关,基底节区则主要与脂质沉积有关。结论:不同时间、部位出1现的短T信号产生的病理机制不同;出血是影响短T信号强度演变规律的主要因素。Objective: To observe the progressive changes and verify the related pathological mechanism of high signal intensity on T1WI after brain ischemia in rat models. Methods: Forty-six male Wistar rats were used for the rat models of middle cerebral artery occlusion(MCAO). Follow-up MR examination was applied to observe the time that T1 shortening appeared, and the position of short T1 signal. HE staining, Perls staining and electric microscopic examination were applied to observe the pathological changes of short T1 signal. Results: The short T1 signal was more often seen in cortical region than in basal ganglia region. The intensity of short T1 signal was different at different time(F=3.746, P<0.05). The histological changes of short T1 signal were hemorrhage, lipid-laden macrophage, denatured protein and myelinolysis. Short T1 signal in cortical region at early stage was mainly related to hemorrhage, short T1 signal in basal ganglia was induced by lipid-laden macrophages. Conclusion: The pathological mechanism of short T1 signal was different in different time of MCAO and different position. Hemorrhage was the main factor which influenced the intensity of short T1 signal.

关 键 词：脑缺血 磁共振成像 

分 类 号：R743.31[医药卫生—神经病学与精神病学] R445.2[医药卫生—临床医学]