目的 研究巴曲酶注射液對改進光化學法致栓塞性腦梗死家兔模型的改善作用。方法 將家兔隨機分為假手術組，模型組，巴曲酶注射液高、低（0.005、0.015 BU/kg）劑量組，采用光化學法致家兔栓塞性性腦梗死模型，并觀察應用巴曲酶注射液對模型的改善效果。結果 改進光化學法造成腦梗死后，各組動物均表現(xiàn)出腦血流量下降，造模后120 min模型組，巴曲酶注射液高、低劑量組較假手術組同期下降均超過50%，同時出現(xiàn)神經(jīng)功能受損等腦梗死癥狀，說明模型科學可靠。給予巴曲酶注射液0.005、0.015 BU/kg后可以不同程度地增加腦血流量，減少神經(jīng)功能損害程度，縮小腦梗死范圍。亦可使纖維蛋白原（FIB）含量明顯降低，組織型纖溶酶原激活劑（t-PA）含量不同程度明顯增加，而且無明顯腦出血不良反應。結論 建立一種改進的光化學法致栓塞性腦梗死家兔模型，方法成功，適用于溶栓藥物評價研究，同時，巴曲酶注射液可以改善此模型受損的神經(jīng)功能，縮小腦梗死范圍。

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.