Author + information
- Received January 19, 1987
- Revision received November 18, 1987
- Accepted December 3, 1987
- Published online April 1, 1988.
- Andrew Thomson, MB,
- Peter J Fletcher, MB, PhD,
- Phillip J Harris, MB, DPhil, FACC,
- Ben Freedman, MB, PhD and
- David T Kelly, MB, FACC∗
- ↵∗Address for reprints: David T. Kelly, MB, Hallstrom Institute of Cardiology, Royal Prince Alfred Hospital, Missenden Road, Campendown 2050, New South Wales, Australia.
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−5·102(p < 0.01) and significantly increased iliofemoral blood flow from 0.34 ± 0.04 to 0.57 ± 0.11 liters/min (p < 0.05). Systemic vascular resistance was reduced from 19 ± 1 to 13 ± 1 dynes-s-cm−5·102(p < 0.001) and cardiac output increased significantly from 4.7 ± 0.3 to 5.8 ± 0.5 liters/min (p < 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−5·102and 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/mm, p < 0.05) and systemic vascular resistance remained significantly reduced (8 ± 1 to 5 ± 1 dynes-s-cm−5·102; p < 0.001). The proportion of cardiac output distributed to the working tower 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.
☆ This work was supported in part by grants from the National Health and Medical Research Council of Australia, Canberra, Australian Capital Territory and the Clive and Vera Ramaciotti Foundation, Sydney, New South Wales, Australia.
- Received January 19, 1987.
- Revision received November 18, 1987.
- Accepted December 3, 1987.