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Exhaled nitric oxide during incremental and constant workload exercise in chronic cardiac failure
S L Lovell1, H Stevenson, I S Young
1Department of Medicine, Royal Victoria Hospital, Belfast, UK.
European Journal of Clinical Investigation
|February 26, 2000
Summary
Impaired nitric oxide (NO) production does not limit exercise in chronic congestive cardiac failure (CCF). Lower NO during maximal exercise may reflect an overactive system in heart failure patients.
Area of Science:
- Cardiovascular Physiology
- Respiratory Medicine
- Exercise Science
Background:
- Nitric oxide (NO) is a vasodilator produced by the pulmonary vascular endothelium.
- Normally, exercise increases cardiac output and decreases pulmonary vascular resistance.
- Impaired NO production in chronic congestive cardiac failure (CCF) may contribute to exercise intolerance.
Purpose of the Study:
- To quantify nitric oxide (NO) production during rest and exercise in patients with CCF.
- To compare NO production in CCF patients with healthy controls.
- To investigate the role of NO in exercise limitation in CCF.
Main Methods:
- Quantified NO production (V NO) in 12 CCF patients and 12 controls.
- Measurements were taken at rest, during incremental exercise, and during constant workload exercise.
- Plasma nitrate levels were also measured.
Main Results:
- CCF patients showed reduced V NO during incremental exercise compared to controls (381 vs. 777 nL min-1).
- V NO was similar between groups during constant workload exercise (353 vs. 389 nL min-1).
- Plasma nitrate levels were higher in CCF patients and unaffected by exercise.
Conclusions:
- Impaired NO-mediated pulmonary vasodilatation does not seem to cause exercise limitation in CCF.
- Reduced NO production during maximal exercise in CCF may indicate an already activated system.
- Further research is needed to understand NO's role in heart failure pathophysiology.