© 2003 European Society of Cardiology
Nitric oxide exhalation correlates with ventilatory response to exercise in patients with heart disease
a Gunma Prefectural Cardiovascular Center 3-12, Kameizumi, Maebashi, Gunma 371-0004, Japan
b The Cardiovascular Institute Tokyo, Japan
* Corresponding author. Tel.: +81-27-269-7455; fax: +81-27-269-1492. E-mail address: h-adachi{at}ops.dti.ne.jp
| Abstract |
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Aims: It is controversial whether or not pulmonary nitric oxide (NO) production, reflected in the end-tidal alveolar NO concentration, is diminished in patients with heart failure. Since pulmonary perfusion is regulated by NO production, decreased NO production in the pulmonary vasculature is assumed to result in diminished lung perfusion and further increases in ventilation–perfusion mismatch. The aim of this study is to investigate whether exhaled NO correlates with both exercise-induced hyperpnea and exercise tolerance in patients with heart disease.
Methods and Results: Forty-two patients with heart disease were enrolled (history of prior myocardial infarction (n=19), dilated cardiomyopathy (n=2), hypertensive heart disease (n=5) and prior open-heart surgery (n=16)). During cardiopulmonary exercise testing, exhaled air was collected and end-tidal NO (ETNO) was measured using a chemiluminescent method. Peak ETNO was found to correlate positively with both ventilatory anaerobic threshold (r=0.468) and peak VO2 (r=0.562). The VE-CO2 slope, which reflects the ventilatory response to exercise, correlated negatively with peak ETNO (r=–0.588).
Conclusion: These data indicate that NO exhalation correlates, inversely, with the ventilatory response to exercise and directly with exercise intolerance, although the weakness of the correlation coefficient suggests there may be other possible mechanisms.
Key Words: Nitric oxide Exercise hyperpnea VE-VCO2 slope Chronic heart failure
Received November 20, 2002; Revised January 30, 2003; Accepted June 16, 2003
There are no potential conflicts of interest with this paper.
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