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背景:磁共振波谱(MRS)可在活体状态下无创地检测脑组织的代谢变化,可补充弥散加权成像单一从形态上识别梗死区脑组织之不足。目的:探讨超急性脑梗死的代谢特点及演变规律,为超急性期溶栓治疗和神经保护剂的使用提供病理生理学依据。设计:随机对照的实验研究。地点和材料:实验地点为重庆医科大学神经病学研究所。选择健康家兔12只,体质量2.0～2.5kg,雌雄不限,由重庆医科大学动物中心提供。随机分成大脑中动脉闭塞(MCAO)组7只,假手术组5只,干预:采用1.5T超导MR成像仪,Probe2000多体素MRS软件包进行扫描。MCAO组,选取缺血后0.5,1,2,3,4和6h时间点对梗死区及其镜像区进行MRS分析。主要观察指标:N-乙酰门冬氨酸(NAA)、磷酸肌酸和肌酸(Pcr+cr)、胆碱类复合物(Cho)和乳酸(Lac)的含量。结果:假手术组双侧代谢物对称分布。在MCAO组缺血0.5h时梗死区即可检测到Lac,为0.56±0.32,随缺血时间延长呈上升趋势,6h时升至2.36±0.24;NAA和Pcr+cr,随缺血时间延长呈下降趋势,除1h,各时间点均较镜像区降低;Cho缺血3h内保持稳定,4h和6h时间点,Cho低于镜像区。结论:梗死区脑组织无氧代谢在超急性期持续存在,神经元损伤及能量代谢障碍始于缺血后2h,细胞膜及髓鞘的破坏始于缺血后4h。
BACKGROUND: Magnetic resonance spectroscopy (MRS) can detect the metabolic changes of brain tissue noninvasively in living state, and can supplement the deficiencies of single weighted morphological identification of infarcted brain tissue by diffusion-weighted imaging. Objective: To investigate the metabolic characteristics and evolution of hyperacute cerebral infarction and to provide pathophysiological evidence for the use of hyperacute thrombolytic therapy and neuroprotective agents. Design: Randomized controlled experimental study. Venue and Materials: The experimental site was Institute of Neurology, Chongqing Medical University. Select 12 healthy rabbits, body weight 2.0 ~ 2.5kg, male or female, provided by the Animal Center of Chongqing Medical University. Randomly divided into middle cerebral artery occlusion (MCAO) group 7, sham operation group 5, intervention: using 1.5T superconducting MR imager, Probe2000 multi-element MRS software package for scanning. MCAO group, select the ischemic 0.5, 1, 2, 3, 4 and 6h time point infarction area and its mirror image MRS analysis. MAIN OUTCOME MEASURES: Content of NAA, Pcr + cr, Cho and lactate (Lac). Results: Symmetrical distribution of bilateral metabolites in sham operation group. In the MCAO group, 0.5g ± 0.32 of Lac could be detected in the infarct zone at 0.5h after ischemia, rising with the prolongation of ischemia and rising to 2.36 ± 0.24 at 6h; NAA and Pcr + cr increased with the prolongation of ischemia Declining trend, except for 1h, was lower than the mirrored area at all time points; Cho remained stable within 3h of Cho ischemia, Cho was lower than the mirror area at 4h and 6h. Conclusion: The anaerobic metabolism of brain tissue in infarction area persists during hyperacute phase. The damage of neurons and energy metabolism start 2h after ischemia, and the destruction of cell membrane and myelin begins 4h after ischemia.