Joshi P I, Dalal J J, Ruttley M S, Sheridan D J, Henderson A H
Br Heart J. 1981 Apr;45(4):457-9. doi: 10.1136/hrt.45.4.457.
We studied the acute effects of nifedipine on left ventricular function and haemodynamics at constant heart rate in patients on beta-blocker therapy. Nifedipine significantly depressed left ventricular peak dP/dt and peak dP/dt x P-1. Nifedipine also significantly reduced systemic vascular resistance: this was associated with decreased systolic blood pressure and increased left ventricular stroke output, with slight non-significant increases of ejection fraction and mean circumferential shortening velocity. There was no change in left ventricular end-diastolic pressure. This clinical study shows that nifedipine increases cardiac output in association with arterial dilatation despite evidence for a negative inotropic effect. Such intrinsic negative inotropic effects would normally be masked by compensatory sympathetic activity.
我们研究了硝苯地平对接受β受体阻滞剂治疗的患者在恒定心率下左心室功能和血流动力学的急性影响。硝苯地平显著降低了左心室最大dp/dt和最大dp/dt×P-1。硝苯地平还显著降低了体循环血管阻力：这与收缩压降低和左心室搏出量增加有关，射血分数和平均圆周缩短速度略有增加但无统计学意义。左心室舒张末期压力无变化。这项临床研究表明，尽管有负性肌力作用的证据，但硝苯地平与动脉扩张相关联，可增加心输出量。这种内在的负性肌力作用通常会被代偿性交感神经活动所掩盖。
