Horikawa Y, Naruse S, Hirakawa K, Tanaka C, Nishikawa H, Watari H
J Cereb Blood Flow Metab. 1985 Jun;5(2):235-40. doi: 10.1038/jcbfm.1985.30.
The energy state of the brain during and after transient cerebral ischemia was examined in rats by in vivo measurement of 31P-nuclear magnetic resonance (NMR) spectra using a topical magnetic resonance spectrometer. EEGs and regional CBF (rCBF) were monitored on the same ischemic models. Immediately after the induction of ischemia, the height of the ATP and phosphocreatine peaks in the spectrum began to decrease with a concurrent increase of the inorganic phosphate (Pi) peak. The calculated pH from the chemical shift of Pi decreased during ischemia. The EEG pattern became flat immediately after ischemic induction. The rCBF decreased below the sensitivity level of the measuring instrument. With 30-min ischemia, the 31P-NMR spectrum returned to a normal pattern rapidly after recirculation. However, recovery of the EEG was delayed. The rCBF after recirculation showed postischemic hyperemia followed by hypoperfusion. In cases of 120-min ischemia, none of the spectra showed recovery. Thus, we could investigate the dynamic process of pathophysiological changes occurring in the ischemic brain in vivo.
利用局部磁共振波谱仪通过体内测量31P-核磁共振(NMR)波谱,对大鼠短暂性脑缺血期间及之后的脑能量状态进行了研究。在相同的缺血模型上监测脑电图(EEGs)和局部脑血流量(rCBF)。缺血诱导后立即出现,波谱中ATP和磷酸肌酸峰的高度开始下降,同时无机磷酸盐(Pi)峰升高。根据Pi的化学位移计算出的pH值在缺血期间下降。缺血诱导后脑电图模式立即变平。rCBF下降至测量仪器的灵敏度水平以下。缺血30分钟后,再灌注后31P-NMR波谱迅速恢复正常模式。然而,脑电图的恢复延迟。再灌注后的rCBF表现为缺血后充血,随后是灌注不足。在缺血120分钟的情况下,所有波谱均未显示恢复。因此,我们能够在体内研究缺血性脑中发生的病理生理变化的动态过程。