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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.

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