Am. J. Respir. Crit. Care Med., Volume 156, Number 3, September 1997, 800-806

Nitric Oxide Inhalation During Exercise in Chronic Obstructive Pulmonary Disease

NÚRIA ROGER, JOAN A. BARBERÁ, JOSEP ROCA, IRENE ROVIRA, FEDERICO P. GÓMEZ, and ROBERT RODRIGUEZ-ROISIN

Serveis de Pneumologia i Al.lergia Respiratòria i d'Anestesiologia, Hospital Clínic, Universitat de Barcelona, Barcelona, Spain

Patients with chronic obstructive pulmonary disease (COPD) may develop hypoxemia and pulmonary hypertension when exercising. To investigate whether inhaled nitric oxide (NO), a selective pulmonary vasodilator, modifies the changes induced by exercise in pulmonary hemodynamics and gas exchange in COPD, we studied nine patients (FEV₁ = 39 ± 2% predicted), at rest and at submaximal exercise, during breathing of room air and NO (40 ppm). NO inhalation decreased pulmonary artery pressure (Ppa) both at rest and during exercise (analysis of variance [ANOVA] p < 0.05). However, the effect of NO on Pa_O2 was different at rest than during exercise. At rest, NO decreased Pa_O2 from 72 ± 3 mm Hg to 65 ± 2 mm Hg, due to an increase in ventilation-perfusion ( A/) inequality (dispersion of blood flow distribution from 0.9 ± 0.1 to 1.1 ± 0.1). During exercise, Pa_O2 decreased during breathing of room air (5 ± 3 mm Hg), whereas it remained essentially unchanged during inhalation of NO (+2 ± 3 mm Hg), with both changes being significantly different (p < 0.05). A/ relationships improved during exercise during breathing of both room air and NO, as a result of a reduction in the dispersion of ventilation distribution. Moreover, NO administered on exertion contributed to redistribute blood flow from alveolar units with low A/ ratios to units with normal ratios (p < 0.05). We conclude that in patients with COPD, the inhalation of NO during exercise moderately reduces pulmonary hypertension, and that in contrast with the effects of such inhalation at rest, it may prevent the exercise-associated decrease of Pa_O2. This effect is probably explained by a preferential distribution of inhaled NO during exercise to well-ventilated alveolar units with faster time constants and normal A/ ratios.

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