Bettinger R, Winkelmann B, Schupp S, Kaltenbach M, Bussmann W D
Abteilung für Kardiologie, Universität Frankfurt/Main.
Dtsch Med Wochenschr. 1993 Jun 25;118(25):927-31. doi: 10.1055/s-2008-1059407.
To elucidate the mechanism of anti-ischaemic and anti-anginal action of angiotensin-converting-enzyme inhibitors, a randomized double-blind study was undertaken in 30 consecutive patients (27 men, 3 women; mean age 58 [28-70] years) with stable angina and at least 50%, angiographically well demonstrated, stenosis of one of the main coronary artery branches. They received an intracoronary infusion of either 0.5 mg captopril (n = 16) or of a placebo (n = 14) to see whether in this form of application the drug could cause an acute dilatation of a coronary stenosis. The diameter before captopril administration was 1.40 +/- 0.63 mm, while 1, 5 and 10 min after infusion it was 1.49 +/- 0.58 mm, 1.30 +/- 0.54 mm and 1.41 +/- 0.59 mm (not significant). There was also no significant difference between captopril and the placebo. The absence of effect with captopril may be due to insufficient liberation of endothelium-derived relaxing factor in an arteriosclerotic coronary segment.
为阐明血管紧张素转换酶抑制剂的抗缺血和抗心绞痛作用机制，对30例连续入选的稳定型心绞痛患者（27例男性，3例女性；平均年龄58[28 - 70]岁）进行了一项随机双盲研究，这些患者造影显示至少一支主要冠状动脉分支狭窄达50%且狭窄情况良好。他们接受了冠状动脉内输注0.5毫克卡托普利（n = 16）或安慰剂（n = 14），以观察在这种给药方式下药物是否能引起冠状动脉狭窄的急性扩张。卡托普利给药前直径为1.40 +/- 0.63毫米，输注后1、5和10分钟分别为1.49 +/- 0.58毫米、1.30 +/- 0.54毫米和1.41 +/- 0.59毫米（无显著差异）。卡托普利与安慰剂之间也无显著差异。卡托普利无效果可能是由于动脉粥样硬化冠状动脉段中内皮衍生舒张因子释放不足。
