Thomson A, Fletcher P J, Harris P J, Freedman B, Kelly D T
Hallstrom Institute of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia.
J Am Coll Cardiol. 1988 Apr;11(4):837-42. doi: 10.1016/0735-1097(88)90220-3.
The short-term effects of sublingual nifedipine (20 mg) on cardiac output and its distribution at rest and during exercise were evaluated by measurement of iliofemoral blood flow and cardiac output in 10 men with stable angina pectoris controlled by metoprolol. At rest, nifedipine significantly decreased iliofemoral vascular resistance from 294 +/- 36 to 165 +/- 29 dynes.s.cm-5.10(2) (p less than 0.01) and significantly increased iliofemoral blood flow from 0.34 +/- 0.04 to 0.57 +/- 0.11 liters/min (p less than 0.05). Systemic vascular resistance was reduced from 19 +/- 1 to 13 +/- 1 dynes.s.cm-5.10(2) (p less than 0.001) and cardiac output increased significantly from 4.7 +/- 0.3 to 5.8 +/- 0.5 liters/min (p less than 0.05). Mean arterial pressure decreased significantly and heart rate increased significantly. During maximal upright bicycle exercise during nifedipine therapy, iliofemoral vascular resistance and leg blood flow were unchanged compared with control (23 +/- 2 versus 21 +/- 3 dynes.s.cm-5.10(2) and 4.7 +/- 0.5 versus 4.4 +/- 0.6 liters/min), cardiac output remained significantly increased (12.8 +/- 0.8 to 15.2 +/- 1.2 liters/min, p less than 0.05) and systemic vascular resistance remained significantly reduced (8 +/- 1 to 5 +/- 1 dynes.s.cm-5.10(2); p less than 0.001). The proportion of cardiac output distributed to the working lower limbs was significantly reduced at all exercise levels. In summary, nifedipine caused a redistribution of cardiac output by vasodilating nonexercising vascular beds without altering the locally mediated vasodilation in exercising muscle. In patients with coronary artery disease given nifedipine therapy, an increase in exercise tolerance is due to relief of myocardial ischemia rather than to increased peripheral oxygen delivery.
通过测量10名服用美托洛尔控制稳定型心绞痛的男性患者的髂股血流量和心输出量，评估了舌下含服硝苯地平（20毫克）对静息和运动时的心输出量及其分布的短期影响。静息时，硝苯地平显著降低髂股血管阻力，从294±36降至165±29达因·秒·厘米⁻⁵·10²（p<0.01），并显著增加髂股血流量，从0.34±0.04升至0.57±0.11升/分钟（p<0.05）。全身血管阻力从19±1降至13±1达因·秒·厘米⁻⁵·10²（p<0.001），心输出量显著增加，从4.7±0.3升至5.8±0.5升/分钟（p<0.05）。平均动脉压显著降低，心率显著增加。在硝苯地平治疗期间进行最大强度直立自行车运动时，与对照组相比，髂股血管阻力和腿部血流量无变化（分别为23±2与21±3达因·秒·厘米⁻⁵·10²以及4.7±0.5与4.4±0.6升/分钟），心输出量仍显著增加（12.8±0.8至15.2±1.2升/分钟，p<0.05），全身血管阻力仍显著降低（8±1至5±1达因·秒·厘米⁻⁵·10²；p<0.001）。在所有运动水平下，分配到工作下肢的心输出量比例均显著降低。总之，硝苯地平通过扩张非运动血管床导致心输出量重新分布，而不改变运动肌肉中局部介导的血管舒张。在接受硝苯地平治疗的冠心病患者中，运动耐力的增加是由于心肌缺血的缓解而非外周氧输送的增加。
