【作者】 李飞；

【导师】 李树清；

【作者基本信息】 昆明医学院 ， 病理学与病理生理学， 2006， 硕士

【摘要】 目的：研究不同脑温(亚低温、常温及高温)对树鼩局部脑缺血海马CA1区内皮细胞生长因子(vascular endothelial growth factor，VEGF)表达的影响，探讨缺血时脑温对VEGF表达的影响及其机制，为临床缺血性脑损伤后的低温后处理的脑保护提供新的依据。方法：建立光化学诱导树鼩皮层脑缺血模型，于缺血后6小时采用局部恒温控温装置维持脑温在亚低温(31～32℃)、常温(36～37℃)和高温(39～40℃)三种不同温度状态持续1h。于缺血后24h及72h处死动物，用免疫组化染色方法染色及图像分析仪测定海马CA1区VEGF表达的不同强度；用电子显微镜观察缺血后24h及72h海马内质网和线粒体的超微结构变化。结果：局部脑缺血后海马CA1区VEGF表达随温度的增加而减弱，亦随时间的延长而减弱；其中以72h时31℃组VEGF的表达下降最为明显(P＜0.01)。海马CA1区神经元的坏死情况表现为：24h时随着温度的减低，海马CA1区神经元坏死减少；31℃组缺血侧呈现随时间延长坏死细胞增多；40℃组随时间的变化缺血侧坏死细胞先增多后减少，对侧则出现相反改变；其缺血侧超微结构显示：随时间的延长超微结构的改变加重。结论：在脑缺血后早期VEGF的表达可能与其直接发挥对神经元细胞的保护作用有关，其次低温对脑缺血的保护作用在脑缺血的早期有明显意义，而在缺血的晚期则可能加重脑缺血的损伤，低温脑保护的意义在于延长脑缺血治疗时间窗。更多还原

【Abstract】 OBJECTIVE: To observe the change of vascular endothelial growth factor (VEGF) expression of different temperature(subhypothermia, normal temperature and hyperthermia) after cerebral thrombosis in hippocampus CAl area of Tree Shrew. To explore the mechanisms of VEGF expression in different Brain-temperature after cerebral thrombosis. To illuminate the effect of the temperature in thrombotic cerebral ischemia and provide the pathophysiologic clues for clinical hypothermia posttreamtent after cerebral ischemia. METHODS: The focal thrombotic cerebral ischemia was induced by photochemical reaction in tree shrews. Different temperature was initiate 6 hours after ischemia, temperature varied from subhypothermia(31℃ ~ 32℃) , normal temperature(36 ℃ ~ 37 ℃ ) and hyperthermia(39℃~40℃), duration 1 hour by focal homeothermia equipment. The absorbance of VEGF expression in neuron of hippocampus CAl area was detected by immunohistochemistry in 24h, 72h after focal cerebral ischemia, using high definition image analysis. The ultramicrostructure of mitochondrion, endoplasmic reticulum change in hippocampus were observed with electronic microscope 24h、 72h after cerebral ischemia. RESULTS: VEGF expressions increased in neuron of hippocampus CAl area at subhypothermia group and reduce at hyperthermia group, and increase in 24h, reduce in 72h, especially in 31℃ group decreased obviously at 72h. The number of cellular necrosis increased at 24h within neuron of hippocampus CAl area at hyperthermia group and reduce at subhypothermia group, and increase at 72h within neuron of the ipsilateral ischemia hippocampus CAl area at subhypothermia group and reduce at 24h; whereas the number ofcellular necrosis increased at 24h in hyperthermia group and reduce at 72h; in contrast to更多还原