RESUMO
AIM: To observe the effects of cimetidine(Cim) on platelet function and thrombosis. METHODS: After incubated with Cim in vitro , rat platelets were activated with ADP or thrombin. The platelet aggregation, platelet malondialdehyde(MDA) formation, platelet intracellular free calcium([Ca 2+ ] i), and thromboxane B 2 (TXB 2) were measured. The effects of Cim on electric-induced thrombosis in rat carotid artery were examined. RESULTS: Cim potentiated ADP induced platelet aggregation , increased the thrombin induced [Ca 2+ ] i and MDA formation, decreased TXB 2. Also, Cim shortened the duration of electric-stimulated occlution time in rat carotid artery. CONCLUSION: Cim increased platelet function and accelerated thrombosis.
RESUMO
In the in vitro model of thrombolysis designed by ourselves, urokinase (500 000~ 5 000 000IU ? L-1) reduced the weight of artificial thrombi in a way of dose-dependence. At the level of 2 000 000 IU ? L-1, the action reached the peak. On the contrary, defibrase (6. 25~25 IU ? L-1) dose-relatedly increased the thrombus weight. After defibrinogenation in platelet-poor plasma by addition of porcine thrombin (100 000 IU ? L-1) , defibrase no longer increased the thrombus weight, whereas in comparison with saline, defibrase still showed no apprciable reduction in thrombus weight. The findings hinted that defibrase may have no direct thrombolytic property.