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大白鼠１８只随机分为３组（每组６只）：假手术组、对照组及东菱克栓酶组（８ＢＵ／ｋｇ）。用４条血管关闭的全脑缺血再灌注模型，全脑缺血３０ｍｉｎ后再灌注６ｈ，观察ＣＡ＿１区海马锥体神经细胞光镜及超微结构变化，结果发现：光镜及超微结构的变化在东菱克栓酶组中显著较对照组轻，而且光镜定量分析发现东菱克栓酶组的神经细胞存活率为８７．３２％，而对照组仅５６．４２％，在受损的神经细胞中，有严重坏死变性者在东菱克栓酶组中仅７．５３％，而对照组高达３０．３３％，为东菱克栓酶组之４倍。以上从形态学上证明东菱克栓酶对脑缺血再灌注损伤确具有保护作用。
Eighteen rats were randomly divided into 3 groups (6 in each group): sham operation group, control group and glibenclamide group (8BU / kg). The model of global cerebral ischemia-reperfusion with 4 blood vessels was closed. After 30 min of global ischemia, reperfusion was performed for 6 h. The light and ultrastructural changes of hippocampal pyramidal neurons in CA 1 area were observed. The results showed that light microscopy and ultrastructure The changes were significantly lighter than those in the control group, and the quantitative analysis by light microscopy showed that the survival rate of Bromhizoma treatment group was 87.32%, while that of the control group was only 56.42% Of the nerve cells, those with severe necrosis degenerated only 7.53% in the group, while the control group was 30.33%, which was 4 times more than that of the other groups. The above morphologically proved that Tongluke thrombin on cerebral ischemia-reperfusion injury indeed have a protective effect.