Exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in COPD with pulmonary hypertension

<p>Abstract</p> <p>Background</p> <p>Endothelin-1 (ET-1) and Nitric Oxide (NO) are crucial mediators for establishing pulmonary artery hypertension (PAH). We tested the hypothesis that their imbalance might also occur in COPD patients with PAH.</p> <p>Method...

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Main Authors: Dragonieri Silvano, Cardone Rosa, Gadaleta Felice, Di Gioia Giuseppe, Seccia Teresa, Maniscalco Mauro, Scoditti Cristina, Carratu Pierluigi, Pierucci Paola, Spanevello Antonio, Resta Onofrio
Format: Article
Language:English
Published: BMC 2008-09-01
Series:BMC Pulmonary Medicine
Online Access:http://www.biomedcentral.com/1471-2466/8/20
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spelling doaj-1a446c39708e407a97fa2ed76590c0312020-11-25T00:31:56ZengBMCBMC Pulmonary Medicine1471-24662008-09-01812010.1186/1471-2466-8-20Exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in COPD with pulmonary hypertensionDragonieri SilvanoCardone RosaGadaleta FeliceDi Gioia GiuseppeSeccia TeresaManiscalco MauroScoditti CristinaCarratu PierluigiPierucci PaolaSpanevello AntonioResta Onofrio<p>Abstract</p> <p>Background</p> <p>Endothelin-1 (ET-1) and Nitric Oxide (NO) are crucial mediators for establishing pulmonary artery hypertension (PAH). We tested the hypothesis that their imbalance might also occur in COPD patients with PAH.</p> <p>Methods</p> <p>The aims of the study were to measure exhaled breath condensate (EBC) and circulating levels of ET-1, as well as exhaled NO (FENO) levels by, respectively, a specific enzyme immunoassay kit, and by chemiluminescence analysis in 3 groups of subjects: COPD with PAH (12), COPD only (36), and healthy individuals (15). In order to evaluate pulmonary-artery systolic pressure (PaPs), all COPD patients underwent Echo-Doppler assessment.</p> <p>Results</p> <p>Significantly increased exhaled and circulating levels of ET-1 were found in COPD with PAH compared to both COPD (p < 0.0001) only, and healthy controls (p < 0.0001). In COPD with PAH, linear regression analysis showed good correlation between ET-1 in EBC and PaPs (r = 0.621; p = 0.031), and between arterial levels of ET-1 and PaPs (r = 0.648; p = 0.022), while arterial levels of ET-1 inversely correlated with FEV<sub>1</sub>%, (r = -0.59, p = 0.043), and PaPs negatively correlated to PaO<sub>2 </sub>(r = -0.618; p = 0.032). Significantly reduced levels of FENO were found in COPD associated with PAH, compared to COPD only (22.92 ± 11.38 vs.35.07 ± 17.53 ppb; p = 0.03). Thus, we observed an imbalanced output in the breath between ET-1 and NO, as expression of pulmonary endothelium and epithelium impairment, in COPD with PAH compared to COPD only. Whether this imbalance is an early cause or result of PAH due to COPD is still unknown and deserves further investigations.</p> http://www.biomedcentral.com/1471-2466/8/20
collection DOAJ
language English
format Article
sources DOAJ
author Dragonieri Silvano
Cardone Rosa
Gadaleta Felice
Di Gioia Giuseppe
Seccia Teresa
Maniscalco Mauro
Scoditti Cristina
Carratu Pierluigi
Pierucci Paola
Spanevello Antonio
Resta Onofrio
spellingShingle Dragonieri Silvano
Cardone Rosa
Gadaleta Felice
Di Gioia Giuseppe
Seccia Teresa
Maniscalco Mauro
Scoditti Cristina
Carratu Pierluigi
Pierucci Paola
Spanevello Antonio
Resta Onofrio
Exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in COPD with pulmonary hypertension
BMC Pulmonary Medicine
author_facet Dragonieri Silvano
Cardone Rosa
Gadaleta Felice
Di Gioia Giuseppe
Seccia Teresa
Maniscalco Mauro
Scoditti Cristina
Carratu Pierluigi
Pierucci Paola
Spanevello Antonio
Resta Onofrio
author_sort Dragonieri Silvano
title Exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in COPD with pulmonary hypertension
title_short Exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in COPD with pulmonary hypertension
title_full Exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in COPD with pulmonary hypertension
title_fullStr Exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in COPD with pulmonary hypertension
title_full_unstemmed Exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in COPD with pulmonary hypertension
title_sort exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in copd with pulmonary hypertension
publisher BMC
series BMC Pulmonary Medicine
issn 1471-2466
publishDate 2008-09-01
description <p>Abstract</p> <p>Background</p> <p>Endothelin-1 (ET-1) and Nitric Oxide (NO) are crucial mediators for establishing pulmonary artery hypertension (PAH). We tested the hypothesis that their imbalance might also occur in COPD patients with PAH.</p> <p>Methods</p> <p>The aims of the study were to measure exhaled breath condensate (EBC) and circulating levels of ET-1, as well as exhaled NO (FENO) levels by, respectively, a specific enzyme immunoassay kit, and by chemiluminescence analysis in 3 groups of subjects: COPD with PAH (12), COPD only (36), and healthy individuals (15). In order to evaluate pulmonary-artery systolic pressure (PaPs), all COPD patients underwent Echo-Doppler assessment.</p> <p>Results</p> <p>Significantly increased exhaled and circulating levels of ET-1 were found in COPD with PAH compared to both COPD (p < 0.0001) only, and healthy controls (p < 0.0001). In COPD with PAH, linear regression analysis showed good correlation between ET-1 in EBC and PaPs (r = 0.621; p = 0.031), and between arterial levels of ET-1 and PaPs (r = 0.648; p = 0.022), while arterial levels of ET-1 inversely correlated with FEV<sub>1</sub>%, (r = -0.59, p = 0.043), and PaPs negatively correlated to PaO<sub>2 </sub>(r = -0.618; p = 0.032). Significantly reduced levels of FENO were found in COPD associated with PAH, compared to COPD only (22.92 ± 11.38 vs.35.07 ± 17.53 ppb; p = 0.03). Thus, we observed an imbalanced output in the breath between ET-1 and NO, as expression of pulmonary endothelium and epithelium impairment, in COPD with PAH compared to COPD only. Whether this imbalance is an early cause or result of PAH due to COPD is still unknown and deserves further investigations.</p>
url http://www.biomedcentral.com/1471-2466/8/20
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