摘要
目的 对比研究慢性前脑缺血致血管性痴呆 (VD)大鼠额叶、颞叶皮质、海马及皮质下白质区的病理学变化 ,探讨血管性痴呆发病的病理基础。方法 采用双侧颈总动脉永久结扎方法制备慢性前脑缺血致 VD大鼠动物模型 ;通过常规 HE及 L FB染色 ,对比观察缺血后不同时间点大鼠额、颞叶皮质、海马区及皮质下白质的形态学改变 ;应用 HPIAS- 10 0 0高清晰彩色病理图文分析系统进行图像分析 ,检测皮质下白质神经纤维脱失情况。结果 HE染色结果显示 :缺血 1个月时额、颞叶皮质及海马区以锥体细胞缺血的改变为主 ,逐渐转变为锥体细胞凝固性坏死、变性、脱失及星形胶质细胞增生 ,少数大鼠额叶出现梗死灶 ;缺血 1个月起实验组大鼠皮质下白质神经纤维疏松、断裂、脱失 ,且有随缺血时间延长而逐渐加重的倾向 ;图像分析显示缺血 1个月实验组大鼠脑白质神经纤维脱失 ,出现囊泡样改变并逐渐增重。结论 进行性的额、颞叶皮质、海马神经元退变以及皮质下白质损害是 VD的病理基础 ,且白质区的损害要早于皮质。
Objective To constract study on the frontal cortex,temporal lobe and Hippocampus with subcortical white matter neuropathology changes of vascular dementia(VD) rats after chronic ischemia. Methods We adopted the permanent occlusion of bilateral common carotid arteries in Wistar rats to produce the chronic forebrain ischemia; Brain samples with HE and LFB staining from frontal lobe,temporal lobe,hippocampus and the white matter were examined with light microscopic methods at 1, 2, 3 and 4m after the operation;The abnormalities of white matter nerve fibre bundle were quantified with an image-analysis system. Results The pyramidal cells of frontal cortex,temporal lobe and hippocampus appeared ischemic changes, such as pyknosis, denaturation, necrosis and degeneration; small vessels proliferation; the proliferation of gliacytes generally existed to form glial nodes; damages of the nerve fibers and myelin sheath were found in the white matter under the cortical layer. The changes mentioned above became severer with the elapse of time. Conclusion The pyramidal neurons of rats decreased progessively and leukoaraiosis after chronic cerebral hypoperfusion are the basic neuropathology of VD,and the change of white matteris occures ealier.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2004年第5期403-405,共3页
Journal of Apoplexy and Nervous Diseases