Background and Purpose - Mild brain hypothermia significantly alleviates damage after focal ischemia, although the mechanism of this protection remains poorly defined. In the present study, we tested the hypothesis that mild hypothermia would protect cortex from early deterioration of ion homeostasis and loss of excitability associated with reperfusion after focal ischemia. Methods - Cortical extracellular potassium ion activity ([K+](o)) and the response of [K+](o) to direct cortical stimulation was measured both in the ischemic core and in the ischemic penumbra of normothermic and mildly hypothermic (31.5°C to 32°C) rats after distal middle cerebral artery occlusion (MCAO) and reperfusion. Results - The response of [K+](o) during MCAO was similar in normothermic and hypothermic animals. However, within 1 hour of reperfusion, [K+](o) in the ischemic core region of normothermic animals showed incomplete recovery and was refractory to direct cortical stimulation. [K+](o) in hypothermic animals returned to preischemic levels on reperfusion and continued to respond to direct cortical stimulation. Mild hypothermia prevented extensive infarction 24 hours after transient MCAO. Conclusions - The data suggest that transient focal ischemia is accompanied by early disturbances of potassium ion homeostasis during reperfusion, which are accompanied by loss of excitability and which may contribute ultimately to cortical infarction.
- Cerebral infarction
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine