Brain extracellular ion composition and EEG activity following 10 minutes ischemia in normo- and hyperglycemic rats.

Hyperglycemia severely impairs the outcome from cerebral ischemia. In order to sort out whether impaired brain ion homeostasis contributes extracellular "K+], [Ca++], and [H+] concentrations, [K+]e, [Ca++]e and [H+]e, of the brain cortex, as well as the EEG, were monitored during and after 10 minutes of complete cerebral ischemia in normo- and hyperglycemic rats. In both groups, the EEG-activity disappeared in 10-20 seconds of ischemia, at a time when [K+]e, [Ca++]e and [H+]e started to increase. After about 1.5 min, [K+]e showed an abrupt increase and [Ca++]e a steep decrease in the normoglycemic group. In the hyperglycemic group the same event took place after about 3 min of ischemia. pHe decreased to 6.6 and 6.1 in the normoglycemic and hyperglycemic group, respectively. Following the ischemic episode [K+]e reached pre-ischemic level after 4 min, [Ca++]e after 13 min, and [H+]e after 30 min in both groups. Recovery of the EEG, however, was clearly different in the 2 groups. EEG-activity reappeared later in the hyperglycemic group and showed after one hour a pattern of burst-suppression activity while the normoglycemic group showed asynchronous activity resembling the control pattern. It is concluded that high glucose content in brain prior to ischemia - and hence lower brain pH during ischemia - does not interfere with the return of normal extracellular ion composition after cerebral ischemia, whereas the return and pattern of EEG activity is severely affected.