Gyngell M L, Busch E, Schmitz B, Kohno K, Back T, Hoehn-Berlage M, Hossmann K A
Max-Planck-Institut für neurologische Forschung, Abteilung für experimentelle Neurologie, Köln, Federal Republic of Germany.
NMR Biomed. 1995 Aug;8(5):206-14. doi: 10.1002/nbm.1940080505.
Focal cerebral ischaemia was produced in 11 rats by permanent occlusion of the right middle cerebral artery (MCA) using a suture model modified to enable manipulation with the animals in situ in an NMR spectrometer. The development of the ischaemic insults and the resultant infarcts were observed for up to 6 h by localized 1H MRS and diffusion-weighted MRI while performing continuous monitoring of electroencephalogram and extracellular DC potential. The ischaemic areas were depicted as regions of hyperintensity in the diffusion-weighted images. Signals due to lactate became visible in the 1H spectra after MCA occlusion indicating the onset of anaerobic glycolysis. A depletion of N-acetylaspartate was seen in all animals post-occlusion. Transient or stepwise increases of lactate were observed to occur coincidentally with the events of spontaneous transient peri-infarct depolarization detected by the electrophysiological measurements. Expansion of the ischaemic area delineated in the diffusion-weighted images also accompanied peri-infarct depolarizations. These observations are consistent with transient peri-infarct depolarization playing a role in the growth of infarcts.
采用改良的缝合模型,通过永久性闭塞11只大鼠的右侧大脑中动脉(MCA)来制造局灶性脑缺血,该模型能够在核磁共振光谱仪中对处于原位的动物进行操作。在持续监测脑电图和细胞外直流电位的同时,通过局部1H磁共振波谱(MRS)和扩散加权磁共振成像(MRI)观察缺血损伤的发展以及由此产生的梗死灶,长达6小时。缺血区域在扩散加权图像中表现为高信号区。MCA闭塞后,乳酸信号在1H谱中可见,表明无氧糖酵解开始。闭塞后所有动物均出现N-乙酰天门冬氨酸耗竭。观察到乳酸的短暂或逐步增加与通过电生理测量检测到的自发性短暂梗死周围去极化事件同时发生。扩散加权图像中描绘的缺血区域扩大也伴随着梗死周围去极化。这些观察结果表明,短暂性梗死周围去极化在梗死灶扩大中起作用。