JACC
HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
 QUICK SEARCH:   [advanced]


     


J Am Coll Cardiol, 1986; 8:1461-1466
© 1986 by the American College of Cardiology Foundation
This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Choong, C.
Right arrow Articles by Kelly, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Choong, C.
Right arrow Articles by Kelly, D.

Effects of nifedipine on arterial oxygenation at rest and during exercise in patients with stable angina

CY Choong, GS Roubin, WF Shen, PJ Harris, SD Anderson, and DT Kelly

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)


This article has been cited by other articles:


Home page
ANN INTERN MEDHome page
A. Matsumoto, S.-i. Momomura, S. Sugiura, H. Fujita, T. Aoyagi, M. Sata, M. Omata, and Y. Hirata
Effect of Inhaled Nitric Oxide on Gas Exchange in Patients with Congestive Heart Failure: A Randomized, Controlled Trial
Ann Intern Med, January 5, 1999; 130(1): 40 - 44.
[Abstract] [Full Text] [PDF]




HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
Copyright © 1986 by the American College of Cardiology Foundation.