We have located links that may give you full text access.
Clinical Trial
Journal Article
Randomized Controlled Trial
Nitric oxide inhalation reduces pulmonary tidal volume during exercise in severe chronic heart failure.
American Heart Journal 1997 October
Multiple mechanisms have been proposed to explain the hyperventilation and the limited exercise capacity in congestive heart failure (CHF) including increased intrapulmonary pressures, total pulmonary resistance, and airway abnormalities. We investigated the hypothesis that inhalation of nitric oxide could influence the maximum exercise capacity and excessive ventilatory response to exercise in CHF. Fifteen patients in CHF (mean age 48 +/- 12 years) underwent a control and a nitric oxide inhalation progressive treadmill exercise test with 30 ppm. We determined the maximum oxygen consumptiom (peak VO2), CO2 production (VCO2), minute pulmonary ventilation (VE), respiratory rate, tidal volume (VT), ventilatory equivalent for oxygen (VE/VO2), ventilatory equivalent for carbon dioxide (VE/VCO2), estimated physiologic dead space/tidal volume ratio (VD/VT), VE/VCO2 slope, heart rate, systemic arterial pressure, VE/exercise time slope, and VT/exercise time slope during every incremental exercise. Mean maximum exercise values of heart rate, systolic systemic arterial pressure, diastolic systemic arterial pressure, VD/VT, respiratory rate, peak VO2, VO2/heart rate, VE/CO2, and maximum exercise time were unchanged by inhalation of nitric oxide. There was a strong trend toward reduction of VE/VO2 from 53 +/- 15 to 47 +/- 12 (p = 0.051) and in maximum VE from 58 +/- 21 to 48 +/- 17 L x min(-1) (p = 0.059). Maximum VT decreased from 1639 +/- 556 to 1406 +/- 479 ml (p = 0.04). The VE/VCO2 slope was reduced from 43 +/- 12 to 35 +/- 8 (p = 0.018). Two patients had signs of pulmonary congestion during peak exercise or the recovery period with inhalation of nitric oxide. The VE/exercise time slope and VT/exercise time slope during incremental exercise were reduced by inhalation of nitric oxide, demonstrating a statistically significant minor increase in VE and VT. Inhalation of nitric oxide attenuated the excessive increase in VT response to exercise in CHF. The L-arginine-nitric oxide pathway may be involved in mechanisms contributing to hyperventilation during exercise in CHF.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
A Guide to the Use of Vasopressors and Inotropes for Patients in Shock.Journal of Intensive Care Medicine 2024 April 14
Diagnosis and Management of Cardiac Sarcoidosis: A Scientific Statement From the American Heart Association.Circulation 2024 April 19
Essential thrombocythaemia: A contemporary approach with new drugs on the horizon.British Journal of Haematology 2024 April 9
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app