van Wijngaarden J, Smit A J, de Graeff P A, van Gilst W H, van der Broek S A, van Veldhuisen D J, Lie K I, Wesseling H
Department of Pharmacology/Clinical Pharmacology, University of Groningen, The Netherlands.
J Cardiovasc Pharmacol. 1994 Feb;23(2):240-5.
Cyclooxygenase inhibitors may affect the hemodynamic status of patients with heart failure adversely and may also block the vasodilatory effects of angiotensin-converting enzyme (ACE) inhibitors in such patients. Relatively low doses of the cyclooxygenase inhibitor acetylsalicylic acid (ASA) are now used routinely in ischemic heart disease, the most important cause of heart failure. Therefore, we investigated the hemodynamic interaction between ASA and captopril in heart failure. In a randomized, cross-over study, 13 patients with congestive heart failure (CHF) who were already receiving maintenance treatment with an ACE inhibitor received a single dose of 25 mg captopril combined with 236 mg ASA or placebo. Peripheral blood flow was studied noninvasively by venous occlusion plethysmography of the calves. Liver blood flow was estimated from indocyanine green (ICG) clearance. Administration of captopril alone significantly decreased blood pressure (BP), and ICG clearance. Calf blood flow remained unchanged. However, after arterial occlusion, hyperemic calf blood flow persisted for longer. Captopril alone did not significantly change the plasma levels of the vasodilating prostaglandins PGI2 and PGE2 or the vasoconstricting thromboxane A2 (TXA2). In contrast, captopril combined with ASA reduced the plasma levels of these vasoactive substances, with significant decreases in PGE2 and TXA2 as compared with captopril alone, yet the hemodynamic alterations after captopril plus ASA were similar to those observed after captopril alone. A single antithrombotic dose of ASA (236 mg) in 13 patients with CHF [New York Heart Association (NYHA) class II-IV] undergoing chronic treatment with ACE inhibitors had no discernible effect on hemodynamic status.(ABSTRACT TRUNCATED AT 250 WORDS)
环氧化酶抑制剂可能会对心力衰竭患者的血流动力学状态产生不利影响，并且还可能阻断此类患者中血管紧张素转换酶（ACE）抑制剂的血管舒张作用。相对低剂量的环氧化酶抑制剂乙酰水杨酸（ASA）目前常用于缺血性心脏病，这是心力衰竭的最重要病因。因此，我们研究了ASA与卡托普利在心力衰竭中的血流动力学相互作用。在一项随机交叉研究中，13名已经接受ACE抑制剂维持治疗的充血性心力衰竭（CHF）患者接受了单剂量25mg卡托普利联合236mg ASA或安慰剂治疗。通过小腿静脉阻塞体积描记法对周围血流进行无创研究。通过吲哚菁绿（ICG）清除率估算肝血流量。单独给予卡托普利可显著降低血压（BP）和ICG清除率。小腿血流量保持不变。然而，动脉阻塞后，充血性小腿血流量持续时间更长。单独使用卡托普利并未显著改变血管舒张性前列腺素PGI2和PGE2或血管收缩性血栓素A2（TXA2）的血浆水平。相比之下，卡托普利与ASA联合使用可降低这些血管活性物质的血浆水平，与单独使用卡托普利相比，PGE2和TXA2显著降低，但卡托普利加ASA后的血流动力学改变与单独使用卡托普利后观察到的相似。在13名接受ACE抑制剂慢性治疗的CHF患者[纽约心脏协会（NYHA）II-IV级]中，单剂量抗血栓剂量的ASA（236mg）对血流动力学状态没有明显影响。（摘要截短于250字）
