title: Cerebral extracellular potassium concentration change and cerebral impedance change in short-term ischemia in gerbil.
abstract: 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.
authors.forename: T
authors.initials: T
authors.lastname: Yamaguchi
mesh_terms: 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
chemical_list: D012964:Sodium; D011188:Potassium; D002118:Calcium