Chabielska E, Pawlak R, Golatowski J, Buczko W
Department of Pharmacodynamics, Medical University of Bialystok, Poland.
J Physiol Pharmacol. 1998 Jun;49(2):251-60.
The mechanism by which ACE-Is (angiotensin converting enzyme inhibitors) reduces the rate of coronary thrombosis among patients with left ventricular dysfunction is not known. A potential interaction between the renin-angiotensin system (RAS) and the thrombotic process has been suggested. The goal of the present study was to evaluate the antithrombotic action of drugs which block the RAS by different mechanisms; captopril (50 mg/kg p.o.)-the angiotensin converting enzyme inhibitor and losartan (30 mg/kg p.o.)-the selective AT1 receptor antagonist. The normotensive rats were treated in acute or chronic manner (7 days) and then the arterial thrombosis was induced by insertion of a loop-shaped cannula into the abdominal aorta. The occlusion time (the period during which the loop was totally occluded by thrombus) was significantly prolonged in comparison with the control groups after chronic treatment with captopril (by 46%; p < 0.01) and losartan (by 42%; p < 0.05). Our results provide experimental evidence that the drugs blocking RAS exert an antithrombotic effect in the arterial thrombosis model in rats. This effect was independent from changes in blood pressure and primary hemostasis.
血管紧张素转换酶抑制剂（ACE-Is）降低左心室功能不全患者冠状动脉血栓形成率的机制尚不清楚。有人提出肾素-血管紧张素系统（RAS）与血栓形成过程之间可能存在相互作用。本研究的目的是评估通过不同机制阻断RAS的药物的抗血栓作用；卡托普利（口服50mg/kg）——血管紧张素转换酶抑制剂和氯沙坦（口服30mg/kg）——选择性AT1受体拮抗剂。对血压正常的大鼠进行急性或慢性（7天）治疗，然后通过将环形插管插入腹主动脉诱导动脉血栓形成。与对照组相比，卡托普利（延长46%；p<0.01）和氯沙坦（延长42%；p<0.05）慢性治疗后，闭塞时间（环形插管被血栓完全闭塞的时间段）显著延长。我们的结果提供了实验证据，表明阻断RAS的药物在大鼠动脉血栓形成模型中发挥抗血栓作用。这种作用独立于血压和初级止血的变化。
