Cerebral blood flow does not mediate the effect of brain temperature on recovery of extracellular potassium ion activity after transient focal ischemia in the rat

Temperature plays an important role in determining outcome following both g lobal and focal brain ischemia. After focal ischemia, the degree of infarct ion decreases with mild hypothermia and increases with mild hyperthermia. I n this study, brain extracellular potassium ion activity and local cerebral blood flow were measured in cerebral cortex during 60 min of middle cerebr al artery occlusion and 60 min of re-perfusion. Brain temperature was maint ained at 32-34 degrees C (mild hypothermia), 35.5-36.5 degrees C (normother mia), or 37.5-38.5 degrees C (mild hyperthermia) throughout ischemia and re -perfusion. In normothermic animals and to a greater degree in hyperthermic animals, extracellular potassium ion activity showed delayed secondary ele vation above pre-ischemia values within 40-60 min after re-perfusion. No se condary elevation of extracellular potassium ion activity was observed in h ypothermic animals. There was no difference in cortical blood flow among gr oups with varying brain temperature, indicating that delayed deterioration of brain potassium ion homeostasis was not caused by temperature dependent alteration of cerebral blood flow. The data suggest that loss of potassium ion homeostasis during re-perfusion after focal cerebral ischemia is caused by cellular rather than vascular dysfunction and may reflect secondary inh ibition of energy metabolism. (C) 1999 Elsevier Science B.V. All rights res erved.