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在冠心病患者,血小板的激活可引起并发症。当血小板受刺激时,花生烯酸被环氧化酶转化成不稳定的内过氧化物。血小板中的血栓素合成酶可将内过氧化物转变成具有缩血管和促聚集作用的血栓素A_2(其稳定的终末产物血栓素B_2的血浆水平可用以反映半寿期短的血栓素A_2的产生)。另一方面,内皮细胞中的扩血管和抗聚集作用的前列环素也是从内过氧化物形成。阿司匹林因阻滞环氧化酶而阻滞血栓素A_2和前列环素两者的形成。亚胺唑的衍生物dazoxiben通过选择性抑制血栓素合成酶,减少血栓素A_2的形成而不阻滞环氧化酶和前列环素的产生。因此,dazoxiben可能比阿司匹林能更有
In patients with coronary heart disease, platelet activation can cause complications. When platelets are stimulated, eicosanoids are converted to labile endoperoxides by cyclooxygenase. Thromboxane synthase in platelets converts endoperoxide into vasoconstrictor-stimulating thromboxane A 2 (the plasma level of thromboxane B 2, which is a stable terminal product, can be used to reflect the short half-life of thromboxane A 2 Of production). On the other hand, vasodilators and anti-aggregating prostacyclin in endothelial cells are also formed from endoperoxides. Aspirin blocks the formation of both thromboxane A 2 and prostacyclin due to blockade of cyclooxygenase. Dazoxiben, a derivative of iminozole, blocks the production of cyclooxygenase and prostacyclin by selectively inhibiting thromboxane synthase and decreasing thromboxane A 2 formation. Therefore, dazoxiben may be more than aspirin