Choong C Y, Roubin G S, Shen W F, Harris P J, Kelly D T
Circulation. 1985 Apr;71(4):787-96. doi: 10.1161/01.cir.71.4.787.
In a placebo-controlled, randomized, cross-over, double-blind study of 12 patients with stable exertional angina, we measured at rest and during bicycle exercise the effects of 20 mg of nifedipine administered sublingually on hemodynamics and systemic and regional oxygen extraction and metabolism. Nifedipine decreased systemic vascular resistance by 38% at rest (p less than .001) and by 28% during exercise (p less than .001). Cardiac output increased from 4.6 +/- 0.6 to 6.0 +/- 0.9 liters/min (p less than .001) at rest after nifedipine and from 10.6 +/- 3.7 to 11.8 +/- 3.4 liters/min (p less than .005) during exercise. After nifedipine, the arterial-mixed venous O2 content difference decreased from 4.7 +/- 0.6 to 3.5 +/- 0.5 ml/100 ml (p less than .001) at rest and from 10.5 +/- 1.7 to 8.8 +/- 1.6 ml/100 ml (p less than .001) during exercise. After nifedipine the arterial-iliac venous O2 content difference also decreased at rest, from 5.9 +/- 1.5 to 4.8 +/- 1.7 ml/100 ml (p = .06) but increased during exercise from 13.1 +/- 1.5 to 14.0 +/- 1.8 ml/100 ml (p less than .05). Oxygen consumption was not significantly altered at rest or during exercise. Nifedipine decreased mixed venous carbon dioxide tension (PCO2) during exercise from 53 +/- 3.5 to 50 +/- 4.0 mm Hg (p less than .05) but increased iliac venous PCO2 slightly from 61 +/- 4.6 to 63 +/- 5.2 mm Hg (p less than .01). Exercise pH was not significantly altered, but arterial lactate increased more after nifedipine (2.65 +/- 1.95 mmol/liter placebo, 3.54 +/- 2.74 mmol/liter nifedipine; p less than .05). Thus nifedipine produces similar changes in O2 extraction in mixed venous and iliac venous blood at rest but directionally opposite changes during exercise. The data support the hypothesis that nifedipine does not alter the distribution of cardiac output to the legs at rest, but during dynamic leg exercise reduces the redistribution of cardiac output to the legs. This probably results from the shunting of blood flow away from exercising muscles by the generalized vasodilatation of nifedipine.
在一项针对12例稳定型劳力性心绞痛患者的安慰剂对照、随机、交叉、双盲研究中，我们在静息状态及自行车运动期间，测量了舌下含服20毫克硝苯地平对血流动力学、全身及局部氧摄取与代谢的影响。硝苯地平使静息时全身血管阻力降低38%（p<0.001），运动时降低28%（p<0.001）。静息时硝苯地平治疗后心输出量从4.6±0.6升/分钟增至6.0±0.9升/分钟（p<0.001），运动时从10.6±3.7升/分钟增至11.8±3.4升/分钟（p<0.005）。硝苯地平治疗后，静息时动脉-混合静脉血氧含量差从4.7±0.6毫升/100毫升降至3.5±0.5毫升/100毫升（p<0.001），运动时从10.5±1.7毫升/100毫升降至8.8±1.6毫升/100毫升（p<0.001）。硝苯地平治疗后，静息时动脉-髂静脉血氧含量差也降低，从5.9±1.5毫升/100毫升降至4.8±1.7毫升/100毫升（p = 0.06），但运动时从13.1±1.5毫升/100毫升增至14.0±1.8毫升/100毫升（p<0.05）。静息或运动时氧耗量无显著改变。硝苯地平使运动时混合静脉二氧化碳分压（PCO2）从53±3.5毫米汞柱降至50±4.0毫米汞柱（p<0.05），但髂静脉PCO2略有升高，从61±4.6毫米汞柱升至63±5.2毫米汞柱（p<0.01）。运动时pH无显著改变，但硝苯地平治疗后动脉乳酸升高更多（安慰剂组2.65±1.95毫摩尔/升，硝苯地平组3.54±2.74毫摩尔/升；p<0.05）。因此，硝苯地平在静息时使混合静脉和髂静脉血中的氧摄取产生类似变化，但在运动时产生方向相反的变化。这些数据支持以下假说：硝苯地平在静息时不改变心输出量向腿部的分布，但在动态腿部运动时减少心输出量向腿部的再分布。这可能是由于硝苯地平引起的全身血管扩张使血流从运动肌肉分流所致。
