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在大鼠脑缺血再灌注损伤实验模型上．观察、测定在脑缺血后对海马组织的兴奋性氨基酸及氧自由基的影响、结果显才缺血后GM1显著减少，诱发其细胞外谷氨酸和天门冬氨酸增高。表明脑缺血再灌注损伤与EAA的过度释放和氧自由基的产生密切相关，而GM1对大鼠脑缺血具有保护作用（P＜0.01）。
On experimental model of cerebral ischemia-reperfusion injury in rats. Observed and measured after cerebral ischemia on the excitatory amino acids and oxygen free radicals in hippocampus, the results were significantly reduced after GM1 was significantly reduced, induced extracellular glutamate and aspartate increased. It showed that cerebral ischemia-reperfusion injury is closely related to the excessive release of EAA and the production of oxygen free radicals, while GM1 has a protective effect on cerebral ischemia (P <0.01).