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背景:脑缺血后脑内代谢物会出现异常变化。目的:通过1H磁共振波谱动态观察局灶性脑缺血大鼠脑内一系列生化代谢的改变,客观反映脑缺血恢复期脑内代谢产物的变化规律。设计:随机对照实验。单位:重庆医科大学附属第一医院的神经内科和放射科。材料:实验于2004-04/07在重庆医科大学附属第一医院放射科完成,选择成年Wistar清结级大鼠24只。随机分为对照组,假手术组和脑缺血组,每组8只。方法:脑缺血组以右侧颈内动脉栓塞制作局灶性脑缺血模型。假手术组栓塞线仅插入颈内动脉未深及大脑中动脉的起始处,对照组麻醉后不作任何处理。应用GEsignaHighspeedMRI1.5T超导磁共振波谱仪,缺血组和假手术组于术后30min,1,3,6,12,24h,3,7,15d,1,2个月对脑梗死区域和对侧半球相应区域进行代谢物的波谱分析。对照组也在上述相应的时间点进行检查。主要观察指标:脑梗死区域和对侧半球相应区域乳酸、N-乙酰天冬氨酸、胆碱及肌酸代谢物的变化。结果:参加实验的动物24只,假手术组中途因麻醉过量死亡2只,脑缺血组因脑缺血后严重脑水肿死亡4只,进入结果分析18只大鼠,正常对照组8只,假手术组6只,脑缺血组4只。①正常对照组和假手术组双侧代谢物无异常改变,分布对称。②脑缺血组梗死区N-乙酰基天冬氨酸、胆碱和肌酸均于脑缺血后30min开始升高,3～6h逐渐降低,但梗死区与对照区N-乙酰基天冬氨酸、胆碱和肌酸没有明显差别(P>0.05)。③6h时患侧的N-乙酰基天冬氨酸显著降低,24h达最低水平(45.21±0.37),胆碱和肌酸于3d降到最低(胆碱93.80±0.56,肌酸69.33±0.44),随缺血时间的延长,N-乙酰基天冬氨酸,胆碱和肌酸逐渐增加,尤其是N-乙酰基天冬氨酸增加最明显,2个月时N-乙酰基天冬氨酸较24h增加2.5倍(112.00±0.03,45.21±0.37,t=-3.33,P<0.05)。④患侧最早于脑缺血后10min检测到乳酸(47.27±0.21),随缺血时间的推移,脑梗死区与对应区乳酸均持续增加到1d以上,12h达高峰,3d开始减少,脑梗死区乳酸明显高于对侧(66.83±0.43,44.35±0.35,t=2.739,P<0.05),在1,2个月时乳酸没有再次升高。结论:①1H磁共振波谱能在患侧脑缺血后10min检测到乳酸,可及早反映动物脑缺血后脑内代谢产物的改变。②1H磁共振波谱能客观定量化反映脑缺血恢复期脑内代谢物的异常。
Background: There are abnormal changes in brain metabolites after cerebral ischemia. OBJECTIVE: To dynamically observe the changes of a series of biochemical metabolism in the brain of focal cerebral ischemia rats by 1H magnetic resonance spectroscopy, and to objectively reflect the changes of brain metabolites in cerebral ischemic recovery period. Design: Randomized controlled experiment. Unit: Department of Neurology and Radiology, the First Affiliated Hospital of Chongqing Medical University. MATERIALS: The experiment was performed in the Department of Radiology, the First Affiliated Hospital of Chongqing Medical University from April 2004 to July 2007. Twenty-four adult Wistar rats were selected. Randomly divided into control group, sham operation group and cerebral ischemia group, 8 rats in each group. Methods: The focal cerebral ischemia model was established by right internal carotid artery embolization in cerebral ischemia group. The sham-operated group’s embolization line was inserted only into the internal carotid artery not deep and the beginning of the middle cerebral artery. The control group received no treatment after anesthesia. Application of GEsignaHighspeedMRI1.5T superconducting magnetic resonance spectroscopy, ischemic group and sham operation group at 30min, 1,3,6,12,24 h, 3,7,15 d, 1,2 months after cerebral infarction area and Spectral analysis of metabolites in the corresponding regions of the hemisphere. The control group was also examined at the appropriate time points above. MAIN OUTCOME MEASURES: Changes of lactate, N-acetylaspartate, choline and creatine metabolites in the corresponding regions of cerebral infarction and contralateral hemisphere. RESULTS: Twenty-four animals were enrolled in the experiment, two died from over-anesthesia in the sham-operation group, four died from severe cerebral edema after cerebral ischemia. 18 rats were included in the analysis, and 8 were normal control group. Six sham operation group and four cerebral ischemia group. ① normal control group and sham operation group no abnormal changes in bilateral metabolites, distribution symmetry. (2) N-acetyl-aspartate, choline and creatine in infarct area of cerebral ischemia group began to increase at 30min after cerebral ischemia and gradually decreased at 3 ~ 6h, but N-acetyl aspartate There was no significant difference in the amino acids, choline and creatine (P> 0.05). The levels of N-acetyl-aspartate in the affected side decreased significantly at 6h (45.21 ± 0.37), the levels of choline and creatine dropped to the minimum at 3d (93.80 ± 0.56 of choline and 69.33 ± 0.44 of creatine) With the prolongation of ischemic time, N-acetyl aspartate, choline and creatine gradually increased, especially N-acetyl aspartate increased most significantly. At 2 months, N-acetyl aspartate 2.5-fold more than 24h (112.00 ± 0.03,45.21 ± 0.37, t = -3.33, P <0.05). ④ The ipsilateral as early as in 10min after cerebral ischemia detected lactic acid (47.27 ± 0.21), with the passage of time, cerebral infarction and lactic acid areas continue to increase to 1d or more, reached the peak at 12h, 3d began to decrease, cerebral infarction The lactic acid in the area was significantly higher than that in the contralateral (66.83 ± 0.43, 44.35 ± 0.35, t = 2.739, P <0.05). Lactic acid did not rise again at 1 and 2 months. Conclusion: ① 1H magnetic resonance spectroscopy can detect lactic acid 10 min after ipsilateral cerebral ischemia, which can reflect the changes of brain metabolites in cerebral ischemia. ② 1H magnetic resonance spectroscopy can objectively quantify the recovery of cerebral ischemia and recovery of brain metabolites abnormalities.