Gotoh O, Yamamoto M, Tamura A, Sano K
Department of Neurosurgery, Toshiba Hospital, Tokyo, Japan.
Acta Neurochir Suppl (Wien). 1994;60:318-20. doi: 10.1007/978-3-7091-9334-1_85.
We investigated the effect of YM737, a monoester of glutathione (GSH), on brain edema and GSH content after occlusion of a middle cerebral artery (MCA) in the rat. The drug possesses stronger radical scavenging activity than GSH itself, and is more effectively transported into cells. Hemispheric water, sodium, and potassium contents were determined at 2.5 and 24 hours after MCA occlusion. The animals received either YM737 or GSH immediately after occlusion. Cerebral GSH content was measured by HPLC after 2.5 hours of ischemia. The increases in water and sodium contents at 2.5 and 24 hours after MCA occlusion were significantly suppressed by YM737. GSH content decreased by 53% in the caudate, and by 22% in the cortex after ischemia. YM737 significantly ameliorated the GSH decrease in the caudate, while administration of GSH showed little effects on the ischemia-induced changes in water, sodium, and GSH contents. The result suggests the role of free radicals in the pathogenesis of ischemic brain edema.
我们研究了谷胱甘肽（GSH）单酯YM737对大鼠大脑中动脉（MCA）闭塞后脑水肿和GSH含量的影响。该药物具有比GSH本身更强的自由基清除活性，并且更有效地转运到细胞中。在MCA闭塞后2.5小时和24小时测定半球水、钠和钾含量。动物在闭塞后立即接受YM737或GSH。缺血2.5小时后通过高效液相色谱法测量脑GSH含量。YM737显著抑制了MCA闭塞后2.5小时和24小时水和钠含量的增加。缺血后尾状核中GSH含量降低了53%，皮质中降低了22%。YM737显著改善了尾状核中GSH的降低，而给予GSH对缺血诱导的水、钠和GSH含量变化几乎没有影响。结果表明自由基在缺血性脑水肿发病机制中的作用。
