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以家兔急性不完全性脑缺血模型，采用“电子自旋共振波谱（ＥｌｅｃｔｒｏｎＳｏｉｎＲｅｓｏｎｃｅ，ＥＳＲ）技术及电子显微镜，对实验性脑缺血组织自由基水平及神经病理进行研究，同时对甘露醇的作用机制进行探讨。结果证实，脑缺血后自由基水平明显增高，神经细胞、星形胶质细胞超微结构发生明显病理改变。而经甘露醇治疗后，自由基水平显著下降，与模型组比较，Ｐ＜０．０１，且大脑皮层细胞损伤程度较模型组明显减轻。这种抑制急性脑组织损伤的作用与甘露醇清除自由基功能及高渗作用密切相关。
The rabbit model of acute incomplete cerebral ischemia was used to study the level of free radicals and neuropathology in experimental cerebral ischemia using "Electron Soluble Resonance (ESR) and electron microscopy. At the same time, The mechanism of action.The results showed that after cerebral ischemia, the level of free radicals was significantly increased, the ultrastructural changes of neurons and astrocytes occurred obvious pathological changes.After mannitol treatment, the level of free radicals decreased significantly with the model group (P <0.01), and the degree of injury of cerebral cortex cells was significantly reduced compared with model group.The effect of inhibiting acute brain injury was closely related to the function of scavenging free radicals and the hypertonic effect of mannitol.