目的 研究巴曲酶注射液对改进光化学法致栓塞性脑梗死家兔模型的改善作用。方法 将家兔随机分为假手术组，模型组，巴曲酶注射液高、低（0.005、0.015 BU/kg）剂量组，采用光化学法致家兔栓塞性性脑梗死模型，并观察应用巴曲酶注射液对模型的改善效果。结果 改进光化学法造成脑梗死后，各组动物均表现出脑血流量下降，造模后120 min模型组，巴曲酶注射液高、低剂量组较假手术组同期下降均超过50%，同时出现神经功能受损等脑梗死症状，说明模型科学可靠。给予巴曲酶注射液0.005、0.015 BU/kg后可以不同程度地增加脑血流量，减少神经功能损害程度，缩小脑梗死范围。亦可使纤维蛋白原（FIB）含量明显降低，组织型纤溶酶原激活剂（t-PA）含量不同程度明显增加，而且无明显脑出血不良反应。结论 建立一种改进的光化学法致栓塞性脑梗死家兔模型，方法成功，适用于溶栓药物评价研究，同时，巴曲酶注射液可以改善此模型受损的神经功能，缩小脑梗死范围。

Objective To study the improvement of Batroxobin Injection on photochemically-induced embolic cerebral infarction model in rabbits. Methods Rabbits were randomly divided into Sham operation, model, high-, and low-dose Batroxobin Injection groups (0.005, 0.015 BU/kg). The embolic cerebral infarction model was induced by photochemical method, then the effect of Batroxobin Injection was observed. Results When the cerebral infarction was caused by improvd photochemical method, the cerebral blood flow reduced in each group. The cerebral blood flow in high- and low-dose Batroxobin Injection groups reduced over 50% at 120 min compared with the Sham group. Even more the damaged nerve function and cerebral infarction were observed, which proved that the model was scientific and reliable. After Batroxobin Injection administration at a dose of 0.005 and 0.015 BU/kg, the cerebral blood flow increased remarkably, and the nerve function and cerebral infarction were also reduced. As well, the research demonstrated that the fibrinogen (FIB) decreased and the tissue-type plasminogen activator (t-PA) increased. More over, there was no remarkable hemorrhage side reaction. Conclusion A model of rabbit focal cerebral infarction with the improvement is established by photochemical method, which is successful and may be reliable in the evaluation of antithrombotic drug research. Meanwhile, Batroxobin Injection could improve the damaged nerve function and narrow the cerebral infarction by this model.