Cerebral extracellular potassium concentration change and cerebral impedance change in short-term ischemia in gerbil.
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.
Yamaguchi
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D000200:Action Potentials; D000818:Animals; D001923:Brain Chemistry; D002118:Calcium / Q000032:analysis / Q000378:metabolism; D002415:Cats; D002540:Cerebral Cortex / Q000032:analysis / Q000503:physiopathology; D004566:Electrodes; D004569:Electroencephalography; D004594:Electrophysiology; D005110:Extracellular Space / Q000032:analysis; D005849:Gerbillinae; D006624:Hippocampus / Q000032:analysis / Q000503:physiopathology; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000503:physiopathology; D011188:Potassium / Q000032:analysis* / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D012964:Sodium; D011188:Potassium; D002118:Calcium