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用Ｗｉｓｔａｒ鼠制作持续性局灶性脑缺血模型，在缺血后１小时内腹腔注射东菱克栓酶（１０ＢＵ／ｋｇ），缺血６小时后测定缺血脑组织局部脑血流（ｒＣＢＦ）并取脑组织进行超微病理检查。结果显示缺血对照组ｒＣＢＦ为７８±２６１８ｍｌ·１００ｇ－１·ｍｉｎ－１，东菱克栓酶组为１１０９±２５５２ｍｌ·１００ｇ－１·ｍｉｎ－１，假手术正常组为１８０１７±１４７ｍｌ·１００ｇ－１·ｍｉｎ－１，三组之间有非常显著性差异（Ｐ＜００１）。电子显微镜检查东菱克栓酶组及缺血对照组均呈现明显缺血坏死性改变，二者之间无明显差异。说明：东菱克栓酶能明显增加动脉持续闭塞缺血脑组织的ｒＣＢＦ，改善局部血液循环，但对持续缺血脑组织的超微结构改变无明显影响。
Wistar rats were used to make the model of persistent focal cerebral ischemia, and intrauterine injection of glibenclamide (10BU / kg) within 1 hour after ischemia and local cerebral blood flow (rCBF ) And brain tissue for ultra-microscopic examination. The results showed that the rCBF of ischemic control group was 78 ± 26.18ml · 100g-1 · min-1 and that of tangling crepe enzyme group was 1109 ± 2552ml · 100g-1 · min-1. The sham operation group was 180.17 ± 14.7ml · 100g-1 · min-1, there was a significant difference between the three groups (P <001). There was no significant difference between the two groups in the ischemic and necrotic changes observed by electron microscopy. It is concluded that batroxobin can significantly increase the rCBF of the ischemic brain tissue and improve the local blood circulation, but it has no significant effect on the ultrastructural changes of persistent ischemic brain tissue.