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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 investigate the mechanism of DF - 521 in thrombolysis and reperfusion injury. Methods The right carotid artery of the gerbils were closed for 1.5 hours with the injured vessel clipped, and then reperfused for 15 hours to release the model of ischemia - reperfusion. The models were induced by DF - 521 and UK respectively. At the same time, Blood and ischemic reperfusion group control. Results The adhesion of leukocytes and endothelial cells was easily seen in cerebral ischemia - reperfusion group, ischemic group and UK intervention group. A large number of deformed erythrocytes and debris were seen in the blood vessels. The brain tissue sections of DF - 521 intervention group Did not find any adhesion phenomenon, and blood vessels filled with intact red blood cells. The results suggest that preventing leukocytes from releasing various inflammatory mediators and avoiding tissue damage may be related to DF - 521 inhibiting the adhesion of leukocytes to endothelial cells. Therefore, DF - 5 2 1 has the effect of attenuating the reperfusion injury at the same time of thrombolysis.