Saito S, Mizumura T, Takayama T, Honye J, Fukui T, Kamata T, Moriuchi M, Hibiya K, Tamura Y, Ozawa Y
2nd Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Cardiovasc Drugs Ther. 1995 Mar;9 Suppl 2:257-63. doi: 10.1007/BF00878473.
The present study was undertaken on 10 patients with angina undergoing percutaneous transluminal coronary angioplasty. The angioplasty procedure consisted of two successive 30-second balloon inflations at 5 minute intervals. After the first inflation, nicorandil (0.1 mg/kg) was given intravenously over a 2-minute period. The second inflation was then performed 3 minutes after the completion of drug administration. Myocardial ischemia was measured as the magnitude of ST-segment elevation on the intracoronary electrocardiogram (intracoronary ECG) recorded from the guidewire. Nicorandil significantly reduced the magnitude of ST-segment elevation. Nicorandil did not change the heart rate-blood pressure product, nor the oxygen saturation of the blood sampled from the great cardiac vein, nor the velocity of coronary blood flow in those patients with no evidence of collaterals. These results favor the conclusion that nicorandil prolongs the intrinsic ability of cardiac myocyte to withstand oxygen deprivation. This salutary effect is possibly due to a direct cellular mechanism because nicorandil did not modify the peripheral and coronary hemodynamic parameters that govern myocardial oxygen consumption.
本研究对10例接受经皮腔内冠状动脉成形术的心绞痛患者进行。血管成形术包括每隔5分钟连续两次30秒的球囊充盈。第一次充盈后，在2分钟内静脉给予尼可地尔（0.1mg/kg）。给药结束3分钟后进行第二次充盈。心肌缺血程度通过从导丝记录的冠状动脉内心电图（冠状动脉内ECG）上ST段抬高幅度来衡量。尼可地尔显著降低了ST段抬高幅度。在无侧支循环证据的患者中，尼可地尔既未改变心率-血压乘积，也未改变从大心静脉采集的血液的氧饱和度，也未改变冠状动脉血流速度。这些结果支持以下结论：尼可地尔可延长心肌细胞耐受缺氧的内在能力。这种有益作用可能归因于直接的细胞机制，因为尼可地尔并未改变控制心肌耗氧量的外周和冠状动脉血流动力学参数。
