Author + information
- Received October 9, 1985
- Revision received June 9, 1986
- Accepted June 25, 1986
- Published online December 1, 1986.
- Christopher Y.P. Choong, MB, PhD1,
- Gary S. Roubin, MB, PhD1,
- Wei Feng Shen, MSc(Med), PhD1,
- Phillip J. Harris, MB, DPhil, FACC1,
- Sandra D. Anderson, PhD1 and
- David T. Kelly, MB, FACC*,1
- ↵*Address for reprints: David T. Kelly, MB, Hallstrom Institute of Cardiology, Royal Prince Alfred Hospital, Sydney, New South Wales 2050, Australia.
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 < 0.05) at rest and from 99 ± 11 to 92 ± 12 mm Hg (p < 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 PaO2was 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 < 0.001) and during submaximal exercise (31 ± 4 versus 33 ± 4 mm Hg, p < 0.03) and maximal exercise (27 ± 3 versus 31 ± 3 mm Hg, p < 0.001).
These findings suggest that nifedipine reduced PaO2at rest and submaximal exercise by increasing ventilation-perfusion imbalance in the lungs, probably as a result of pulmonary vasodilation and increase in cardiac output. No correlation was found between the reduction in rest Pao2and pulmonary vascular resistance, suggesting that other factors were involved.
- Received October 9, 1985.
- Revision received June 9, 1986.
- Accepted June 25, 1986.
- American College of Cardiology Foundation