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目的 探讨不同溶栓治疗时间窗与细胞间粘附分子 - 1(ICAM 1)表达及白细胞浸润的关系。方法 采用自体血栓栓塞大脑中动脉 ,缺血 0 .5小时、1小时或 4小时开始溶栓治疗 ,应用免疫组织化学方法 ,观察缺血 12小时或 2 4小时ICAM 1的表达、白细胞的浸润程度 ;TTC染色测定梗死灶的大小。结果 缺血12小时和 2 4小时 ,4小时溶栓组较 0 .5小时和 1小时溶栓组梗死灶体积明显增大 (P <0 .0 1) ;缺血周边区I CAM 1面密度、浸润白细胞数增多 (P <0 .0 1) ;1小时溶栓组较 0 .5小时溶栓组梗死灶体积增大 (P <0 .0 5 ) ;浸润的白细胞数无显著性差异 (P >0 .0 5 ) ,但ICAM 1面密度增加 (P <0 .0 5 )。缺血 2 4小时与缺血 12小时比较 ,0 .5小时溶栓组ICAM 1面密度减少 (P <0 .0 5 ) ;而 1小时和 4小时溶栓组明显增加 (P <0 .0 5 ,P <0 .0 1)。结论 超早期溶栓治疗可以减少缺血周边区ICAM 1表达及白细胞的浸润 ;白细胞浸润参与了溶栓治疗后的病理生理过程。
Objective To investigate the relationship between different thrombolysis time windows and the expression of intercellular adhesion molecule - 1 (ICAM - 1) and leukocyte infiltration. Methods Thromboembolism of the middle cerebral artery was performed by autologous thromboembolism. Thrombolytic therapy was started at 0.5 hour, 1 hour or 4 hours after ischemia. Immunohistochemistry was used to observe the expression of ICAM 1 at 12 hours or 24 hours after ischemia. The degree of leukocyte infiltration TTC staining was used to determine the size of infarction. Results After 12 hours and 24 hours of ischemia, the volume of infarction in thrombolytic group increased significantly (P <0.01) at 4 hours compared with 0. 5 hours and 1 hour (P <0.01) , The number of infiltrating leukocytes increased (P <0.01); the volume of infarction in thrombolytic group increased (P <0.05) at 1 hour and no significant difference P> 0.05), but the surface density of ICAM 1 increased (P <0.05). Compared with the 12-hour ischemia, 0.5-hour ICAM-1 reduced the density of thrombolytic group (P <0.05), while the levels of ICAM-1 increased significantly at 1 hour and 4 hours (P <0. 0) 5, P <0. 01). Conclusion Ultra-early thrombolytic therapy can reduce ICAM-1 expression and leukocyte infiltration in peripheral region of ischemic area. Leukocyte infiltration is involved in the pathophysiological process after thrombolysis.