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慢性局灶脑缺血区血管周细胞的形态学观察
引用本文:雷万龙,袁群芳,董志宏,姚志彬.慢性局灶脑缺血区血管周细胞的形态学观察[J].神经解剖学杂志,2001,17(4):373-376,T064.
作者姓名:雷万龙  袁群芳  董志宏  姚志彬
作者单位:中山医科大学,人体解剖学教研室,
基金项目:广东省博士后基金(粤学位办[1997]35号)资助项目
摘    要:为了深入研究血管周细胞的生物学特性和在脑缺血病理过程中的形态学变化规律 ,对不同缺血时间的大鼠大脑皮质缺血区和尾壳核区的血管周细胞的变化进行了免疫组织化学探查。结果显示 :(1)在脑缺血早期 (3 d,1周 ) ,ED2阳性反应的血管周细胞呈圆形或卵圆形 ,无明显的突起。数量增加的阳性细胞主要位于大脑皮质缺血灶外围的血管周围 ,并随血管走行而分布 ,缺血灶中央区的阳性细胞数量少。在缺血侧尾壳核 ,阳性细胞的数量明显增加 ,呈卵圆形或杆状 ,阳性细胞大多数位于尾壳核的实质内 ,少数位于血管壁内 ;(2 )在脑缺血后期 (4周 ,6周 ) ,大脑皮质缺血灶外周的 ED2阳性细胞的数量、形态和分布形式与脑缺血早期相比 ,也无明显变化 ;但在脑缺血灶的中央区有大量的 ED2阳性反应细胞 ,呈圆形 ,无明显突起 ;脑缺血后期 ED2阳性细胞主要位于尾壳核外侧区 ,其数量与缺血早期无明显的变化 ,但细胞形态变化显著 ,大多数细胞胞体肥大并有 2~ 3个明显的突起。脑缺血后期 ,在侧脑室脉络丛出现大量 ED2阳性反应的细胞 ,其胞体肥大 ,并有多个突起。结果表明 :慢性局灶脑缺血导致大脑皮质缺血区和尾壳核区的血管周细胞发生特征性的形态学改变。提示 ,血管周细胞与慢性脑缺血病理变化有联系

关 键 词:局灶脑缺血  血管周细胞  大脑皮质  尾壳核  大鼠

A MORPHOLOGICAL EXPLORATION FOR PERIVASCULAR CELLS IN CHRONIC FOCAL ISCHEMIC BRAIN IN RATS
Lei Wanlong,Yuan Qunfang,Dong Zhihong,Yao Zhibin.A MORPHOLOGICAL EXPLORATION FOR PERIVASCULAR CELLS IN CHRONIC FOCAL ISCHEMIC BRAIN IN RATS[J].Chinese Journal of Neuroanatomy,2001,17(4):373-376,T064.
Authors:Lei Wanlong  Yuan Qunfang  Dong Zhihong  Yao Zhibin
Abstract:To further study both biological characteristic and morphological alterative pattern of perivascular cells in focal ischemic brain, the alterations of perivascular cells were immunohistochemically explored both in ischemic cortex and caudoputamen of adult SD rats of per time point. The results showed that (1) at the early duration of ischemia (3 d~1 w), ED2 positive perivascular cells of round or ovoid shape lacked processes and increased in number around the cortic ischemic foci and were distributed along vasculatures, but they were less in the ischemic core. ED2 positive cells of ovoid or rod shape, which were in the parenchyma of ischemic caudoputamen and in the vascular wall, increased apparently in number. (2) At the late duration of ischemia (4~6 w), the number, shape and distribution of ED2 positive cells were not apparently different around the cortic ischemic foci in contrast to those of the early duration of ischemia, but a large number of ED2 positive cells of round shape and lacked processes were recruited in the core of ischemic cortex. ED2 positive cell number in the lateral region of ischemic caudoputamen was not changed, but the remarkable alterations of the cellular forms occurred, in which hypertrophic somas and 2~3 stouter processes were shown. Meanwhile, a number of ED2 positive cells becoming hypertrophy and possessing several processes were found accumulating in the choroid plexus of lateral ventricle at the late duration of ischemia. The above results confirmed that chronic focal ischemia was able to induce the morphological alteration of ED2 positive perivascular cells in the ischemic cortex and caudoputamen and indicated that perivascular cells participated in the pathological process of cerebral ischemia.
Keywords:focal cerebral ischemia  perivascular cell  cerebral cortex  caudoputamen  rat
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