Lijnen P, Boelaert J, Van Eeghem P, Daneels R, Schurgers M, De Jaegere P, Van der Stichele E, Vincke J, Verschueren L J, Amery A
J Cardiovasc Pharmacol. 1984 May-Jun;6(3):455-9. doi: 10.1097/00005344-198405000-00013.
Using a double-blind procedure, 29 patients with a recent myocardial infarction were randomly allocated to a placebo group (n = 14) and to a group receiving aspirin, 300 mg three times a day (n = 15) over 7 days. No change in renal function was observed in either treatment group. Compared with the placebo group, the 24-h urinary excretion of prostaglandin E2 (PGE2) was significantly suppressed in the aspirin group, but the urinary kallikrein activity was unchanged. These results contrast with our previous study of similar patients, in which sulfinpyrazone decreased renal function, as well as the urinary PGE2 and kallikrein excretions. These divergent effects of aspirin and sulfinpyrazone on urinary kallikrein activity could explain the different trends in renal function observed early after myocardial infarction.
采用双盲程序,将29例近期发生心肌梗死的患者随机分为安慰剂组(n = 14)和接受阿司匹林治疗组(n = 15),后者每天3次,每次300 mg,持续7天。两个治疗组均未观察到肾功能变化。与安慰剂组相比,阿司匹林组前列腺素E2(PGE2)的24小时尿排泄量显著降低,但尿激肽释放酶活性未改变。这些结果与我们之前对类似患者的研究结果形成对比,在之前的研究中,磺吡酮降低了肾功能以及尿PGE2和激肽释放酶排泄量。阿司匹林和磺吡酮对尿激肽释放酶活性的这些不同作用可以解释心肌梗死后早期观察到的肾功能的不同变化趋势。