NITRIC-OXIDE INHALATION DURING EXERCISE IN CHRONIC OBSTRUCTIVE PULMONARY-DISEASE

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% pred icted), at rest and at submaximal exercise, during breathing of room a ir 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 tha n 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 ((V) over dotA/(Q) over dot) inequality (dispersion of blood flow distribution f rom 0.9 +/- 0.1 to 1.1 +/- 0.1). During exercise, Pa-O2 decreased duri ng breathing of room air (-5 +/- 3 mm Hg), whereas it remained essenti ally unchanged during inhalation of NO (+2 +/- 3 mm Hg), with both cha nges being significantly different (p < 0.05). (V) over dotA/(Q) over dot relationships improved during exercise during breathing of both ro om air and NO, as a result of a reduction in the dispersion of ventila tion distribution. Moreover, NO administered on exertion contributed t o redistribute blood flow from alveolar units with low (V) over dot/(Q ) over dot ratios to units with normal ratios (p < 0.05). We conclude that in patients with COPD, the inhalation of NO during exercise moder ately reduces pulmonary hypertension, and that in contrast with the ef fects of such inhalation at rest, it may prevent the exercise-associat ed decrease of Pa-O2. This effect is probably explained by a preferent ial distribution of inhaled NO during exercise to well-ventilated alve olar units with faster time constants and normal (V) over dotA/(Q) ove r dot ratios.