Suryapranata H
Department of Cardiology, Hospital de Weezenlanden, Zwolle, The Netherlands.
Eur Heart J. 1993 Jul;14 Suppl B:16-21. doi: 10.1093/eurheartj/14.suppl_b.16.
Previous studies have indicated that nicorandil reduces both preload and afterload, clearly distinguishing nicorandil from conventional nitrates, whose predominant action is that of preload reduction. In association with the decrease in afterload following nicorandil, the contractile responses during isovolumic contraction and relaxation improved significantly, indicating that nicorandil does not demonstrate negative inotropic actions. Furthermore, despite a marked decrease in mean aortic pressure after nicorandil, coronary sinus blood flow remains unchanged. Therefore, coronary vasodilatation must have taken place, while myocardial oxygen consumption decreased significantly. The vasodilatory action of nicorandil on the epicardial coronary artery has also been demonstrated in our previous study. Nicorandil, at a dose of either 20 or 40 mg, induces a significant increase in coronary artery diameter favourably by acting not only on the non-stenotic but also on the stenotic coronary segments. In our recent study, the effects of intracoronary nicorandil (6 mu.kg-1) and isosorbide dinitrate (2 mg) on the epicardial coronary arteries were investigated in patients undergoing coronary angioplasty. In non-stenotic coronary artery segments, the mean coronary diameter increased significantly after either nicorandil (+12%) or isosorbide dinitrate (+17%). In stenotic segments, however, increase in the diameter of the obstructed segment by 20% after intracoronary nicorandil was much more pronounced when compared to that of 8% after isosorbide dinitrate. There was a significant additional increase of 13% in the diameter of the obstructed segment when nicorandil was administered following isosorbide dinitrate, while no such additional effect was observed when isosorbide dinitrate was given after nicorandil.(ABSTRACT TRUNCATED AT 250 WORDS)
先前的研究表明,尼可地尔可降低前负荷和后负荷,这使其与传统硝酸盐类药物明显不同,传统硝酸盐类药物的主要作用是降低前负荷。随着尼可地尔使后负荷降低,等容收缩和舒张期间的收缩反应显著改善,这表明尼可地尔不表现出负性肌力作用。此外,尽管尼可地尔使平均主动脉压显著降低,但冠状窦血流量保持不变。因此,必然发生了冠状动脉扩张,同时心肌耗氧量显著降低。我们先前的研究也证实了尼可地尔对心外膜冠状动脉的血管舒张作用。20毫克或40毫克剂量的尼可地尔不仅作用于非狭窄冠状动脉节段,还作用于狭窄冠状动脉节段,从而显著增加冠状动脉直径。在我们最近的研究中,对接受冠状动脉血管成形术的患者研究了冠状动脉内注射尼可地尔(6微克/千克)和硝酸异山梨酯(2毫克)对心外膜冠状动脉的影响。在非狭窄冠状动脉节段,尼可地尔(增加12%)或硝酸异山梨酯(增加17%)给药后,平均冠状动脉直径均显著增加。然而,在狭窄节段,冠状动脉内注射尼可地尔后阻塞节段直径增加20%,比硝酸异山梨酯后的8%更为显著。硝酸异山梨酯给药后再给予尼可地尔,阻塞节段直径显著额外增加13%,而尼可地尔给药后再给予硝酸异山梨酯则未观察到这种额外效应。(摘要截选至250字)