东菱克栓酶、尿激酶对沙土鼠脑缺血再灌注模型白细胞与内皮细胞粘附抑制的实验观察

Leucocyte and endothelial cell adhesion inhibition with DF-521 and UK in Gerbil cerebral ischemia-reperfusion model

目的 探讨东菱精纯克栓酶 (DF - 5 2 1)在溶栓的同时缓解再灌注损伤的机制。方法 以无损伤血管夹夹闭沙土鼠右侧颈总动脉 1.5h ,放开再灌注 1 5h制成缺血再灌注模型 ,分别以DF - 5 2 1、尿激酶 (UK)干预 ,同时设缺血组及缺血再灌注组对照。结果 脑缺血再灌注组、缺血组、UK干预组脑组织切片中极易见到白细胞与内皮细胞的粘附 ,血管中可见大量变形红细胞及碎片 ,DF - 5 2 1干预组脑组织切片中未发现任何粘附现象 ,且血管内充满形态完好的红细胞。结论 提示阻止白细胞释放各种炎症介质 ,避免组织损害 ,可能与DF - 5 2 1抑制白细胞与内皮细胞粘附有关。因此 ,DF - 5 2 1在溶栓的同时尚有减弱再灌注损伤的作用。

Objective To explore the mechanism that DF-521 remits the damage of reperfusion when it dissolutes emboli. Methods The Gerbil scervical general artery was blocked on its right side using an intact serrefine for 1.5 hours,and follow-on reperfusion another 1.5 hours to form ischemia reperfusion model.Then interference with it by using DF-521 and UK was made separately.The group of ischemia was compared with ischemia reinfusion group. Results The leucocyte and endothelial system adhesion was easily seen in the brain tissue slice of cerebral ischemia reperfusion group.In the group of ischemia using UK a large amount of ameboid cells,mainly erythrocytes and pieces could be found.Not any adhesion can be seen in the brain tissue slice of DF-521 group and the blood vessel was filled with perfect erythrocytes. Conclusion Preventing leucocyte releasing all kinds of infammatory factors and avoiding the damage of the system may relate to DF-521 effect on the inhibition of the leucocyte and endolhelial system adherence, so when DF-521 is added to streptokinase,it can reduce the damage of reperfusion.