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高糖对兔早期脑梗死影响的质子磁共振波谱实验研究
引用本文:程敬亮,张勇,杨运俊,张敏,任翠萍,张焱,赵艺蕾. 高糖对兔早期脑梗死影响的质子磁共振波谱实验研究[J]. 河南大学学报(医学版), 2005, 24(1): 9-11
作者姓名:程敬亮  张勇  杨运俊  张敏  任翠萍  张焱  赵艺蕾
作者单位:郑州大学第一附属医院,放射科,河南,郑州,450052;洛阳正骨医院,影像科,河南,洛阳,471002
基金项目:河南省杰出青年科学基金资助项目041200060,河南省医学科技创新人才工程资助项目2003015,河南省重点科技攻关计划资助项目0224630105
摘    要:目的:观察早期兔大脑中动脉阻塞(MCAO)后高血糖模型的质子磁共振波谱(1H-MRS)演变规律。方法:8只新西兰大白兔于MCAO后2h,经腹腔给予50g/L的葡萄糖注射液(5g/kg)。实验动物分别在模型建立前及建立后0.5h、1h、2h、4h、6h、8h、12h和24h进行1H-MRS检查。结果:Naa于加用高糖后0.5h内出现短暂回升,加用高糖1h后达到高峰,加用高糖2h后恢复至加用高糖前的水平,随后持续下降。Cho含量于加用高糖后无明显变化。Cr含量于加用高糖0.5h后开始下降,加用高糖1h后达最低点,随后略有回升,但随着时间的延长,Cr持续下降。Lac于加用高糖后0.5h内迅速升高,1h后即达高峰,随后逐渐恢复至加用高血糖前的水平。结论:高血糖仅能对神经元起到短暂的益处,随时间延长,高血糖反而加重神经元损伤。

关 键 词:磁共振波谱  脑梗死  动物实验
文章编号:1672-7606(2005)01-0009-03

An experimental research of hyperglycemia upon early ischemic infarction with proton magnetic resonance spectroscopy in rabbits
CHENG Jing-liang,ZHANG Yong,YANG Yun-jun,ZHANG Min,REN Cui-ping,ZHANG Yan,ZHAO Yi-lei. An experimental research of hyperglycemia upon early ischemic infarction with proton magnetic resonance spectroscopy in rabbits[J]. Journal of Henan University, 2005, 24(1): 9-11
Authors:CHENG Jing-liang  ZHANG Yong  YANG Yun-jun  ZHANG Min  REN Cui-ping  ZHANG Yan  ZHAO Yi-lei
Affiliation:CHENG Jing-liang 1,ZHANG Yong 1,YANG Yun-jun 1,ZHANG Min 2,REN Cui-ping 1,ZHANG Yan 1,ZHAO Yi-lei 1
Abstract:Objective: To observe the evolution of early cerebral infarction in rabbit model of middle cerebral artery occlusion (MCAO) and hyperglycemia with proton magnetic resonance spectroscopy ( 1H-MRS). Methods: 8 New Zealand rabbits were included in the experiment. The experimental rabbits underwent MCAO and peritoneal injection of glucose 5g/kg. They were examined by MR scanner before operation as well as at 0.5h, 1h, 2h, 2.5h, 3h, 3.5h, 4h and 6h after operation. Results: Naa hoist transitorily in 0.5h after hyperglycemia, and Naa raised to the pinnacle in 1h, it decreased to pre-hyperglycemia level at 2h, and decreased continuously. Cho level did not change after hyperglycemia. Cr level decreased 0.5h after hyperglycemia, and decreased to the lowest at 1h after hyperglycemia, afterward Cr increased a little, but reduced subsequently with the time coursing. Lac level increased dramatically in 0.5h, and increased to its highest in 1h after hyperglycemia, finally returned back to its pre-hyperglycemia level. Conclusion: The neuron cell could only benefit from hyperglycemia transitorily, but with the time going, hyperglycemia would aggravate neuron cell injury.
Keywords:magnetic resonance spectroscopy  cerebral infarction  animal experiment
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