Lei B, Adachi N, Arai T
Department of Anesthesiology and Resuscitology, Ehime University School of Medicine, Japan.
Neurosci Lett. 1997 Jan 31;222(2):91-4. doi: 10.1016/s0304-3940(97)13349-3.
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.
采用微透析结合二氯荧光素氧化荧光测定法，研究了沙土鼠海马在缺血及再灌注过程中细胞外过氧化氢（H2O2）浓度的变化。在常温条件（37.5℃）下，短暂性前脑缺血5或10分钟，在缺血开始后立即导致海马H2O2显著增加。再灌注后，5分钟缺血的沙土鼠中这种升高的持续时间明显短于10分钟缺血的沙土鼠。34℃和30℃的低温均抑制了5分钟缺血沙土鼠在缺血及再灌注过程中H2O2浓度的升高。在10分钟缺血的沙土鼠中，低温延迟了H2O2浓度升高的起始时间，并缩短了H2O2浓度升高的持续时间。低温改善了缺血7天后海马CA1神经元的组织学结果。这些发现表明，低温抑制缺血及再灌注过程中H2O2的产生可能是其脑保护机制之一。
