A Prior Brain Microinjury Attenuates Hypermetabolism Induced by Brain Ischemia-Reperfusion in the Mouse

We have previously shown that a prior brain microinjury improves survival of mice following brain ischemia, though the precise mechanism remains to be determined. The purpose of the present study was to examine the modulatory effects of the brain microinjury on postischemic brain metabolism. Sixty-eight DDY mice were divided into four groups: sham-operated non-ischemia, sham-operated ischemia, brain-injured non-ischemia, and brain-injured ischemia groups. Brain microinjury was induced by vertically inserting a 25-gauge needle into the brain at selected four sites. Seven days after the injury or sham-operation, animals in two ischemia groups were subjected to brain ischemia (60 min occlusion of bilateral carotid arteries). Using 2-[14C] deoxyglucose method, relative metabolic activity of brain regions was measured seven days after brain microinjury or sham operation in two non-ischemia groups and seven days after brain ischemia in the other two ischemia groups. There were no significant differences in relative metabolic activity of any brain region measured when compared between sham-operated and brain-injured animals without ischemia. In mice with sham operation, metabolic activity after ischemia was significantly higher in 8 of 22 brain regions examined that that measured without ischemia (p < .05). In mice with brain microinjury, metabolic activity remained unchanged following brain ischemia in any brain region examined except in the mammilary complex. The minor brain injury it self did not affect regional brain metabolism but attenuated postischemic increase in metabolic activity, suggesting that the ability of an antecedent brain microtrauma to attenuate postischemic hypermetabolism is involved in protection from subsequent ischemic-reperfusion injury.