Zhao H, Asai S, Kanematsu K, Kunimatsu T, Kohno T, Ishikawa K
Department of Pharmacology, Nihon University School of Medicine, Tokyo, Japan.
Neuroreport. 1997 Jul 7;8(9-10):2389-93. doi: 10.1097/00001756-199707070-00057.
Brain hypothermia during ischemia may have a neuroprotective effect on pathological and functional outcomes in vivo. Although a microdialysis study demonstrated that hypothermia decreases glutamate release into the extracellular space, the issue of whether this suppression of the glutamate elevation normally accompanying ischemia is attributable to inhibition of intra-ischemic release or acceleration of post-ischemic re-uptake was not addressed. Recently, we established a real-time method for monitoring glutamate levels in extracellular space, utilizing a dialysis electrode. This method allows detailed analysis of the in vivo dynamics of biphasic glutamate elevation in the extracellular space during the intra-ischemic period and post-ischemic re-uptake. The present results show that post-ischemic hypothermia has little effect on the initial glutamate release, but remarkably enhances post-ischemic glutamate re-uptake.
缺血期间的脑部低温可能对体内的病理和功能结果具有神经保护作用。尽管一项微透析研究表明低温可减少谷氨酸释放到细胞外空间，但这种对通常伴随缺血的谷氨酸升高的抑制是归因于缺血期间释放的抑制还是缺血后再摄取的加速这一问题并未得到解决。最近，我们利用透析电极建立了一种监测细胞外空间谷氨酸水平的实时方法。该方法允许详细分析缺血期间和缺血后再摄取期间细胞外空间双相谷氨酸升高的体内动力学。目前的结果表明，缺血后低温对初始谷氨酸释放影响不大，但显著增强了缺血后谷氨酸的再摄取。
