中文摘要：

目的：观察局灶性脑缺血大鼠血瘀证相关指标的改变，为建立病证结合的脑卒中血瘀证动物模型提供实验依据。方法：采用插线法致大脑中动脉栓塞（MCAO）2h制备局灶性脑缺血大鼠模型，分别于再灌注6、12、24、48、72和168h取血并处死动物取相应标本。检测腹动脉血血液流变学动态变化；采用酶联免疫吸附法（ELISA）和放射免疫竞争法测定脑组织白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF—α）含量；用苏木素-伊红（HE）染色法观察脑细胞的病理形态学变化并进行细胞计数；用原位末端缺刻标记法（TUNEL）检测细胞凋亡情况。结果：与假手术组比较，模型组再灌注12～168h全血黏度和红细胞聚集率明显增高（P〈0.05或P％0．01），再灌注48h时血浆纤维蛋白原含量也显著增高（P〈0.01）。缺血侧脑组织前炎症细胞因子IL-1β水平于再灌注6～24h明显增高，TNF—α含量于再灌注24～48h显著增多（P〈0.05或P〈0．01）；再灌注6～72h脑缺血梗死区细胞数量明显减少，12～72h凋亡细胞大量出现（P均〈0.01）。结论：局灶性脑缺血大鼠模型出现血液流变学指标异常和脑部病变，因此有可能作为脑卒中血瘀证的病证结合动物模型。

英文摘要：

Objective： To investigate the dynamic changes of hemorheology in rat models with focal cerebral ischemia, and explore the possibility of developing disease/syndrome- combined （血瘀证） animal model of stroke and blood stasis syndrome （血瘀证）. Methods： The rat model with focal cerebral ischemia was prepared with middle cerebral artery occlusion （MCAO） induced by thread insertion for 2 hours, then reperfusion was carried out, and at 6, 12, 24, 48, 72 and 168 hours of reperfusion, blood samples were taken and the models were decapitated respectively. The hemorheological indexes of blood drawn from abdominal aorta were measured by automatic hemorheometer. The content of interleukin -1β （IL -1β） and tumor necrosis factor-α （TNF-α） in brain tissue were determined by enzymelabeled immunosorbent assay （ELISA） and radioimmunoassay （RIA）. The pathological change and apoptosis were detected by hematoxylin-eosin staining（HE） and terminal deoxynucleotidyl- transferase mediated dUTP- biotin nick end labeling （TUNEL） method respectively. Results： The whole blood viscosity and erythrocyte aggregation significantly increased in the blood drawn from abdominal aorta during the period of reperfusion for 12- 168 hours after focal cerebral ischemia （P〈0.05 of P〈0. 01）, and the plasma fibrinogen obviously increased at the reperfusion for 48 hours （P〈0. 01）. The level of pro - inflammatory cytokine IL -1β in cerebral cortex evidently elevated during the reperfusion for 6 - 24 hours, and the content of TNF -α significantly increased during the reperfusion for 24 - 48 hours （P〈0. 05 or P〈0. 0l）. The cell count in cerebral infarction area obviously decreased during the reperfusion for 6 - 72 hours and apoptosis increased in a great quantity during the period of reperfusion for 12- 72 hours after cerebral ischemia （all P〈0.01）. Conclusion： Focal cerebral ischemia rat model shows brain disorders and hemorheological abnormality in systemic circulation, suggest