Choong C Y, Roubin G S, Shen W F, Harris P J, Anderson S D, Kelly D T
J Am Coll Cardiol. 1986 Dec;8(6):1461-6. doi: 10.1016/s0735-1097(86)80324-2.
The effects of nifedipine on arterial oxygenation and hemodynamics were studied at rest and during bicycle exercise in 12 men (mean age 55 years, range 41 to 67) with stable exertional angina. The study was conducted double-blind on 2 days, 1 week apart, using a placebo-controlled crossover design. On each day, measurements at rest were made before and 20 minutes after 20 mg sublingual nifedipine or placebo and were followed by measurements made during exercise. Compared with placebo, nifedipine reduced mean arterial pressure, systemic vascular resistance and pulmonary vascular resistance, and increased heart rate and cardiac output at rest and during exercise. It did not alter mean pulmonary artery or pulmonary artery wedge pressures at rest, but decreased them during exercise. Nifedipine decreased arterial oxygen tension (PaO2) from 96 +/- 10 to 90 +/- 13 mm Hg (p less than 0.05) at rest and from 99 +/- 11 to 92 +/- 12 mm Hg (p less than 0.005) at submaximal exercise (33 +/- 21 W), but did not alter it (100 +/- 12 versus 100 +/- 16 mm Hg, p = NS) at maximal exercise (68 +/- 30 W). The reduction in PaO2 was not due to alveolar hypoventilation, because nifedipine did not alter arterial carbon dioxide tension, or to changes in mixed venous oxygen tension, which nifedipine increased at rest (39 +/- 2 versus 43 +/- 3 mm Hg, p less than 0.001) and during submaximal exercise (31 +/- 4 versus 33 +/- 4 mm Hg, p less than 0.03) and maximal exercise (27 +/- 3 versus 31 +/- 3 mm Hg, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
对12名患有稳定型劳力性心绞痛的男性(平均年龄55岁,范围41至67岁),研究了硝苯地平在静息状态和自行车运动期间对动脉氧合和血流动力学的影响。该研究采用安慰剂对照交叉设计,在相隔1周的2天内进行双盲试验。每天,在舌下含服20mg硝苯地平或安慰剂之前和之后20分钟进行静息测量,随后进行运动期间的测量。与安慰剂相比,硝苯地平在静息和运动期间降低了平均动脉压、全身血管阻力和肺血管阻力,并增加了心率和心输出量。它在静息时未改变平均肺动脉压或肺动脉楔压,但在运动期间使其降低。硝苯地平使静息时动脉血氧分压(PaO2)从96±10降至90±13mmHg(p<0.05),在次极量运动(33±21W)时从99±11降至92±12mmHg(p<0.005),但在极量运动(68±30W)时未改变(100±12对100±16mmHg,p=无显著性差异)。PaO2的降低不是由于肺泡通气不足,因为硝苯地平未改变动脉血二氧化碳分压,也不是由于混合静脉血氧分压的变化,硝苯地平在静息时(39±2对43±3mmHg,p<0.001)、次极量运动期间(31±4对33±4mmHg,p<0.03)和极量运动时(27±3对31±3mmHg,p<0.001)使其升高。(摘要截断于250字)