论文部分内容阅读
以往的研究已证实:芦沙坦可阻滞血管壁止血栓烷A_2受体。本实验的目的是评价芦沙坦对人体血小板活性的影响。 血小板取自于15例健康人,年龄26～40岁,含血小板的血浆先用血栓烷A_2同型物U_4 6619或ADP刺激,用光密度变化测定。 结果表明,U_4 6619刺激的血小板聚集很明显以剂量依赖方式被芦沙坦抑制,只在高剂量EXP3174(5×10~(-5)mol/L)时,芦沙坦的主动代谢才能减低U_4 6619诱导的血小板激活。开博通—血管紧张素Ⅰ转换酶抑制剂的一种,则不能减低U_4 6619诱导的血小板亲合。此外,[3H]—U_4 6619与血小板的粘合被芦沙坦竞争性抑制,而高剂量的EXP3174才能降低
Previous studies have shown that: Losartan can block the blood vessel wall thromboxane A 2 receptor. The purpose of this experiment was to evaluate the impact of losartan on human platelet activity. Platelets were obtained from 15 healthy individuals aged 26 to 40 years. Platelet-containing plasma was first stimulated with Thromboxane A 2 isoforms U 4 6619 or ADP, and the changes in optical density were measured. The results showed that platelet aggregation induced by U_4 6619 was significantly inhibited by losartan in a dose-dependent manner. Only at high dose of EXP3174 (5 × 10 -5 mol / L), active metabolism of losartan could reduce U_4 6619 induced platelet activation. Open Broadcom - a kind of angiotensin I converting enzyme inhibitor, can not reduce U_4 6619 induced platelet affinity. In addition, binding of [3H] -U_4 6619 to platelets was competitively inhibited by losartan, whereas high doses of EXP3174 were able to decrease