尿激酶对兔急性血栓后静脉壁形态变化的影响

目的：评估尿激酶溶栓对急性期血管壁炎性反应和静脉壁形态变化的影响。方法：建立兔的急性股静脉血栓模型,将43只兔随机分为溶栓组20只、未溶栓组20只、对照组3只,分别于血栓形成后第1、4、7、21天获取股静脉,通过检测静脉壁平滑肌肌动蛋白、胶原沉积来评估平滑肌增生,内皮层扫描电镜评估内皮细胞损伤情况。结果：平滑肌肌动蛋白及胶原纤维检测提示溶栓组静脉壁增生明显低于未溶栓组, 电镜扫描提示溶栓组内皮细胞 损伤明显低于未溶栓组。结论：尿激酶溶栓能有效地保护内皮层完整,减轻血管壁肌血管增生,但不能阻断其病理改变。

Effect of urokinase on morphological changes of vein wall after acute thrombosis in rabbits

Objective To assess the effect of urokinase on morphological changes of vein wall after acute thrombosis in rabbits. Methods Forty three rabbits were randomly divided into 3 groups: thrombolysis group ( n =20), non thrombolysis group ( n =20) and control group ( n =3). Thethrombosed femoral veins of four rabbits in thrombolysis group anf four rabbits in non thrombolysis group were taken 1, 4, 7, 14, and 21 days after thrombosis. The expression areas of smooth muscle actin and collagen fiber were measured by histochemistry. Scanning electron microscopy was used to observe the damage of endothelial cells. Results The expression area of smooth muscle actin began to increase significantly since day 4 after thrombosis reached the peak value on day 7 in thrombolysis group and non thromlysis group; and then decreased in thombolysis group but remained at a high level in non thrombolysis group. The expression area of smooth muscle actin in thrombolysis group was always less that in non thrombosis group (all P <0.01). The expression area of collagen fiber began to remarkably increase since day 7 after thrombosis in both thrombolysis and non thrombolysis groups, however, being less in the thrombolysis group, and then decreased in thrmbolysis group and remained at a high level in non thrombosis group. Different cellular damages were observed by SEM one day after thrombosis in both thrombosis groups. However, the injurey cells began to be repaired since day 4 in thrombolysis group. Conclusion Thrombolysis with urokinase effectively maintains the integrety of endotheliunm of vein wall and decreases the fibrocellular proliferation of the thrombosed vein, however, fails to stop the pathological changes caused by thrombosis.