Production of endogenous nitric oxide in chronic obstructive pulmonary disease and patients with cor pulmonale - Correlates with echo-doppler assessment

Citation
E. Clini et al., Production of endogenous nitric oxide in chronic obstructive pulmonary disease and patients with cor pulmonale - Correlates with echo-doppler assessment, AM J R CRIT, 162(2), 2000, pp. 446-450
Citations number
43
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
ISSN journal
1073449X → ACNP
Volume
162
Issue
2
Year of publication
2000
Pages
446 - 450
Database
ISI
SICI code
1073-449X(200008)162:2<446:POENOI>2.0.ZU;2-6
Abstract
Exhaled nitric oxide (NO) production in stable chronic obstructive pulmonar y disease (COPD) has been loosely related to the severity of illness, being significantly reduced in the most severe cases. Pulmonary hypertension is associated with lower NO output from the lung. In this study expired NO was measured in patients with severe stable COPD with or without cor pulmonale (CP). Echocardiographic estimates of right heart function, lung function, diffusion capacity, respiratory muscle strength, and arterial blood gases w ere obtained in 34 consecutive patients with stable COPD (mean age, 68 +/- 7 yr). Expired NO was measured by chemiluminiscence to obtain fractional ex haled concentrations at peak (FENOp) and at plateau (FENOpl) points of the single-breath curve and resting NO output ((V)over dot(NO)). All measuremen ts of expired NO output, FENOp, FENOpl and (V)over dot(NO) showed a negativ e correlation with both systolic pulmonary artery pressure (Pspa) (r = -0.5 1, -0.63, and -0.63, respectively, p < 0.01 for all) and right ventricle wa ll dimension (r = -0.41, -0.59, and -0.43, respectively, p < 0.05 for all), but not with any measurement of lung function. When the patients were divi ded according to the Pspa using a cutoff limit of 35 mm Hg, those subjects with CP showed lower FENOp (13.2 +/- 4.0 versus 36.7 +/- 30.8 ppb, p < 0.05 ), FENOpl (5.7 +/- 1.9 versus 8.9 +/- 4.7 ppb, p < 0.05), and (V)over dot(N O) (69.2 +/- 5.6 versus 107.6 +/- 14.6 nl/min, p = 0.02) than did those wit h a normal resting Pspa. NO production from the airways was significantly l ower and inversely related to development of CP in patients with severe COP D. Impaired endothelial release may account for the reduced levels of expir ed NO.