Exhaled nitric oxide during incremental and constant workload exercise in chronic cardiac failure

Background Nitric oxide (NO) is present in exhaled breath and produced by t he pulmonary vascular endothelium as a potent vasodilator. Exercise is norm ally associated with pulmonary vasodilatation and a decrease in pulmonary v ascular resistance to accommodate the increase in cardiac output. If produc tion of NO is impaired in patients with chronic congestive cardiac failure (CCF), this might contribute to their exercise intolerance. Patients and methods We quantified NO production ((V) over dot NO) in 12 pa tients with chronic stable CCF and 12 controls, at rest and during incremen tal cardiopulmonary exercise on a treadmill, and at a later date during con stant workload exercise. Results Patients had reduced (V) over dot NO compared with controls during incremental exercise [381 (180) vs. 777 (275) nL min(-1); mean (SD); P < 0. 0001] but at constant workload (V) over dot NO was similar between the two groups [353 (124) vs. 389 (189) nL min(-1); P= 0.25]. Plasma levels of nitr ate, the stable end-product of NO production, were significantly higher in patients [resting value 46.1 (21.6) vs. 23.0 (10.0) mu M; P = 0.004] and we re not influenced by exercise. Conclusion Impaired NO-mediated pulmonary vasodilatation does not appear to contribute to exercise limitation in CCF Alternatively, the lower NO produ ction observed during maximal exercise in the patient group compared with c ontrols may reflect a reduced incremental response of a system that is alre ady abnormally activated in heart failure.