Schaper Wolfgang
Department of Experimental Cardiology, Max-Planck-Institute, Bad Nauheim, Germany.
Cardiovasc Drugs Ther. 2005 Oct;19(5):357-63. doi: 10.1007/s10557-005-4659-6.
Dipyridamole, developed almost half a century ago, acts by inhibiting nucleoside transport, which increases adenosine levels leading to inhibition of platelet aggregation and vasodilatation mainly in the coronary tree. It is a vaso-protective drug with proven efficacy in the prevention of strokes. Adenosine receptor 2 inhibitory purines, ubiquitously available in food and drink, inhibit the vasomotor effects of dipyridamole but not its action on platelet aggregation. This and the slow build-up of blood levels of dipyridamole after oral application may explain why incidents of drug-induced angina ("coronary steal") were never reported in the prevention trials. The prevention of arterial thrombosis and the positive remodeling of the arterial system (arteriogenesis) by elevated blood flows suggest that dipyridamole may be able to halt the progression of organ manifestations of atherosclerosis. Clinical trials for the secondary prevention of vascular occlusions in other vascular beds should be encouraged.
双嘧达莫大约在半个世纪前研发出来,其作用机制是抑制核苷转运,从而提高腺苷水平,主要在冠状动脉中导致血小板聚集受抑制和血管舒张。它是一种血管保护药物,在预防中风方面已证实有效。食物和饮料中普遍存在的腺苷受体2抑制性嘌呤会抑制双嘧达莫的血管运动作用,但不影响其对血小板聚集的作用。口服后双嘧达莫血药浓度上升缓慢,这两点或许可以解释为何在预防试验中从未报告过药物诱发心绞痛(“冠状动脉窃血”)的事件。通过增加血流量预防动脉血栓形成以及动脉系统的正向重塑(动脉生成)表明,双嘧达莫或许能够阻止动脉粥样硬化器官表现的进展。应鼓励开展针对其他血管床血管闭塞二级预防的临床试验。