The effect of hypothermia on H2O2 production during ischemia and reperfusion: a microdialysis study in the gerbil hippocampus.

The changes in the extracellular concentration of hydrogen peroxide (H2O2) in gerbil hippocampus during ischemia and reperfusion were investigated by microdialysis coupled with fluorometry of dichlorofluorescin oxidation. In a normothermic condition (37.5 degrees C), a transient forebrain ischemia for 5 or 10 min produced a significant increase in hippocampal H2O2 immediately after the start of ischemia. The duration of this elevation after reperfusion was significantly shorter in gerbils subjected to 5 min of ischemia than in those subjected to 10 min of ischemia. Hypothermia at both 34 degrees C and 30 degrees C inhibited the increase in the H2O2 concentration during ischemia and reperfusion in gerbils subjected to 5 min of ischemia. In gerbils subjected to 10 min of ischemia, hypothermia delayed the onset of the increase in the H2O2 concentration and shortened the duration of the elevated H2O2 concentration. Hypothermia improved the histological outcome in the hippocampal CA1 neurons 7 days after ischemia. These findings suggest that the suppression of H2O2 production in ischemia and reperfusion is a possible mechanism of brain protection by hypothermia.