1986 Volume 33 Issue 1 Pages 1-8
Extracellular potassium and calcium ion concentration, field potential (Fp), local EEG and cortical impedance were measured continuously in the cortex and hippocampus of the pentobarbital anesthetized gerbils subjected to 5-minute ischemia produced by bilateral carotid occlusion. Extracellular potassium ([K+]e) and extracellular calcium ([Ca++]e) showed a triphasic change during ischemia followed by a biphasic change after recirculation. The EEG became flat within about 20 seconds. There was a sharp increase in the [K+]e and a sharp decrease in the [Ca++]e, which coincided with the sharp increase in the Fp around one and a half minutes. The impedance increased simultaneously with a large amplitude change of EEG. The [Ca++]e continued to decrease for another 1-2 minutes before returning to the normal values after recirculation whereas the [K+]e began to decrease immediately. The extracellular space (ECS) did not change until depolarization. The rise of the [K+]e and [Ca++]e in the pre-depolarization phase was not explained by the shrinkage of the ECS. The possible explanation for the change of the [Ca++]e in ischemia was discussed.