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[通过体内多核磁共振波谱法对沙鼠脑缺血期间及之后代谢变化的研究]

[Studies of metabolic changes during and following cerebral ischemia in gerbils by in vivo multi nuclear magnetic resonance spectroscopy].

作者信息

Igarashi H

出版信息

Nihon Ika Daigaku Zasshi. 1989 Aug;56(4):339-48. doi: 10.1272/jnms1923.56.339.

Abstract

Cerebral metabolism was investigated in cerebral ischemia in fasted Mongolian gerbils by in vivo magnetic resonance spectroscopy (MRS). Ischemia was induced by bilateral carotid artery occlusion and continued for 30 min. Recovery was achieved by releasing the occlusion. High energy adenylates, free phosphates as well as intracellular pH were measured by 31P-MRS. Cerebral lactate levels were determined by 1H-MRS. Furthermore, extracellular sodium levels were monitored by 23Na-MRS. The results showed that intracellular pH decreased to pH = 6.601 at 7.5-15 min after carotid ligation and was regulated back to pH = 6.670 during ischemia. pH returned to preischemic levels 45 min after ischemia and there was an overshoot (pH = 7.241) in pH levels at 67.5-75 min after recirculation. The accumulation of lactate was slower and the accumulation continued after intracellular pH started to regulate back to normal levels. Lactate decreased following recirculation, but was still higher than the preischemic level at 90 min after recirculation. The results show that changes in intracellular pH is not parallel those in lactate levels, suggesting a different mechanism for regulating intracellular pH. The signal intensity of sodium was dropped before ATP disappeared, and rapidly normalized at 14-26 min after recirculation, at which time ATP had also normalized. This result suggests that the loss of signal intensity of 23Na shows depolarization induced by ischemia and Na-K ATP pump failure.

摘要

通过体内磁共振波谱(MRS)研究了禁食蒙古沙鼠脑缺血时的脑代谢情况。通过双侧颈动脉闭塞诱导缺血,并持续30分钟。通过解除闭塞实现恢复。通过31P-MRS测量高能腺苷酸、游离磷酸盐以及细胞内pH值。通过1H-MRS测定脑乳酸水平。此外,通过23Na-MRS监测细胞外钠水平。结果显示,颈动脉结扎后7.5 - 15分钟,细胞内pH值降至pH = 6.601,在缺血期间又调节回pH = 6.670。缺血后45分钟,pH值恢复到缺血前水平,再灌注后67.5 - 75分钟,pH值出现过冲(pH = 7.241)。乳酸的积累较慢,在细胞内pH值开始调节回正常水平后仍持续积累。再灌注后乳酸减少,但再灌注90分钟时仍高于缺血前水平。结果表明,细胞内pH值的变化与乳酸水平的变化不平行,提示调节细胞内pH值的机制不同。钠的信号强度在ATP消失之前下降,并在再灌注后14 - 26分钟迅速恢复正常,此时ATP也已恢复正常。这一结果表明,23Na信号强度的丧失显示了缺血诱导的去极化和钠钾ATP泵功能衰竭。

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