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目的 观察大鼠脑缺血后脑内组织水分子表观弥散系数(apparentdiffusioncoefficient ,ADC)及乳酸(lactate ,Lac)和N 乙酰基天门冬氨酸(N acetyl aspartate ,NAA)的改变,以及胞二磷胆碱对它们的影响。方法 Wistar大鼠右侧大脑中动脉栓塞制作永久性脑缺血模型,将磁共振弥散加权成像(diffusionweightedimaging ,DWI)异常的区域为1 H磁共振波谱分析(protonmagneticresonancespectroscopy ,1 HMRS)定位。结果 脑缺血组脑缺血6h后患侧Lac升高,2 4h达高峰,3d时开始降低;而NAA于脑缺血6h即有降低,2 4h降到最低,3d后开始升高,7d时接近正常水平,各时间点Lac值和NAA值与对照组相比有显著性差异(P <0 0 5 )。对照组和假手术胞二磷胆碱组无Lac产生,胞二磷胆碱对NAA及ADC值无明显影响。胞二磷胆碱组患侧与健侧的表观弥散系数比率[apparentdiffusioncoefficientratio ,ADCR (ADCR =患侧表观弥散系数 健侧表观弥散系数) ]及患侧ADC值较脑缺血组明显增加(P <0 0 5 ) ,胞二磷胆碱治疗后患侧Lac逐渐降低(P <0 0 5 )以及NAA逐渐升高(P <0 0 5 )。结论 1 HMRS能够反映动物脑缺血后脑内代谢物的改变。胞二磷胆碱能够改善脑缺血后代谢物的变化并减轻脑水肿形成。
Objective To observe the changes of apparent diffusion coefficient (ADC), lactate (Lac) and N acetyl aspartate (NAA) in brain tissue after cerebral ischemia in rats, The effect of choline on them. Methods Permanent cerebral ischemia was induced by embolization of the right middle cerebral artery of Wistar rats. The areas of abnormalities of diffusion weighted imaging (DWI) were determined by 1 HMRS (1 H-NMR). Results After 6h of cerebral ischemia, the Lac in the ipsilateral brain increased and peaked at 24 hours, then began to decrease at 3 days. NAA decreased at 6 hours, decreased to the lowest at 24 hours, then increased at 3 days and increased at 7 days Close to the normal level, at each time point Lac and NAA values compared with the control group were significantly different (P <0 05). There was no Lac production in control group and sham-operated citicoline group. Citicoline had no significant effect on NAA and ADC value. Apparent diffusion coefficient ratio of ipsilateral and contralateral to citicoline group [apparent diffusion coefficient ratio (ADCR)] and ipsilateral ADC value was significantly higher than that of cerebral ischemia group (P <0 05). Laccy decreased gradually (P 0 05) and NAA gradually increased after citicoline treatment (P 0 05). Conclusion 1 HMRS can reflect the changes of brain metabolites in cerebral ischemia. Citicoline can improve the changes of metabolites after cerebral ischemia and reduce the formation of cerebral edema.