目的 建立自體血栓和凝血酶致大鼠局灶性腦梗死模型。方法 采用經(jīng)頸外動(dòng)脈向頸內(nèi)動(dòng)脈注入自體血栓和凝血酶栓塞大鼠大腦中動(dòng)脈的方法，建立局灶性腦梗死模型并觀察重組葡激酶（rSak）對(duì)該模型的改善作用。結(jié)果 注入10 μL自體血栓和50 U凝血酶時(shí)大鼠腦血流量較基礎(chǔ)值降低，出現(xiàn)嚴(yán)重腦梗死神經(jīng)癥狀、較大腦梗死范圍和明顯病理學(xué)改變，為理想模型。rSak 150 kU/kg能提高腦血流量，減少腦神經(jīng)缺陷評(píng)分，縮小腦梗死范圍，減輕病理學(xué)改變。結(jié)論 建立了經(jīng)頸內(nèi)動(dòng)脈注入自體血栓和凝血酶致大鼠局灶性腦梗死模型，并用rSak驗(yàn)證了該模型的穩(wěn)定性及可靠性。

Objective To establish a focal cerebral infarction model by autologous thromb and thrombin. Methods The focal cerebral infarction model was made by infusion of autologous thromb and thrombin from the external carotid artery into the internal carotid artery, and the improvement of rSak to this model was observed. Results After injection of 10 μL autologous thromb and 50 U thrombin, there were reduced rat cerebral blood flow, severe neurological symptoms, cerebral infarction, and obvious pathological changes compared to normal rats, that was thought to be the ideal model. rSak 150 KU/kg could improve the cerebral blood flow, reduce brain neurological symptoms, cerebral infarction, and pathological changes. Conclusion A model focal cerebral infarction model is established by infusion of autologous thromb and thrombin from the external carotid artery into the internal carotid artery, and the stability and reliability of the improvement of this model is observed by rSak.