Stroke, Vol 12, 236-240, Copyright © 1981 by American Heart Association
E Siemkowicz and AJ Hansen
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.
ARTICLES
Brain extracellular ion composition and EEG activity following 10 minutes ischemia in normo- and hyperglycemic rats
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