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Ultrastructural study of the effects of tranexamic acid and urokinase on metastasis of Lewis lung carcinoma.

机译:氨甲环酸和尿激酶对Lewis肺癌转移影响的超微结构研究。

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摘要

Lewis lung carcinoma cells were implanted in the foot-pads of mice and the effects of the plasminogen-plasmin inhibitor tranexamic acid (t-AMCHA) and of the plasminogen activator urokinase on metastasis were examined by electron microscopy. The intravascular tumour cells were not associated with thrombus formation in either control or urokinase-treated mice. Polymerized fibrin deposition around tumour cells and thrombi composed of fibrin and platelets was observed only in the mice given t-AMCHA. This suggests that the inhibition of fibrinolysis by tACC caused fibrin deposition and thrombus formation around intravascular tumour cells, which prevented release of the cells from primary foci to form secondary tumours. On the other hand, fibrinolysis induced by urokinase prevented thrombus formation, and accelerated cell release from primary foci.
机译:将Lewis肺癌细胞植入小鼠脚垫中,并通过电子显微镜检查纤溶酶原-纤溶酶抑制剂氨甲环酸(t-AMCHA)和纤溶酶原激活剂尿激酶对转移的影响。在对照或尿激酶治疗的小鼠中,血管内肿瘤细胞均与血栓形成无关。仅在给予t-AMCHA的小鼠中观察到聚合纤维蛋白在肿瘤细胞周围的沉积以及由纤维蛋白和血小板组成的血栓。这表明tACC对纤维蛋白溶解的抑制导致纤维蛋白沉积和血管内肿瘤细胞周围的血栓形成,这阻止了细胞从原发灶释放而形成继发性肿瘤。另一方面,由尿激酶引起的纤维蛋白溶解可防止血栓形成,并加速细胞从原发灶的释放。

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