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

Pierluigi Carratu, Cristina Scoditti, Mauro Maniscalco, Teresa Seccia, Giuseppe Di Gioia, Felice Gadaleta, Rosa Cardone, Silvano Dragonieri, Paola Pierucci, Antonio Spanevello, Onofrio Resta

Research output: Contribution to journalArticle

Abstract

Background: 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. Methods: 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. Results: 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 FEV1%, (r = -0.59, p = 0.043), and PaPs negatively correlated to PaO2 (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.

Original languageEnglish
Article number20
JournalBMC Pulmonary Medicine
Volume8
DOIs
Publication statusPublished - Sep 26 2008

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Endothelin-1
Pulmonary Hypertension
Chronic Obstructive Pulmonary Disease
Pulmonary Artery
Blood Pressure
Lung
Nitric Oxide
Luminescence
Immunoenzyme Techniques
Endothelium
Linear Models
Epithelium
Regression Analysis

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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Exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in COPD with pulmonary hypertension. / Carratu, Pierluigi; Scoditti, Cristina; Maniscalco, Mauro; Seccia, Teresa; Di Gioia, Giuseppe; Gadaleta, Felice; Cardone, Rosa; Dragonieri, Silvano; Pierucci, Paola; Spanevello, Antonio; Resta, Onofrio.

In: BMC Pulmonary Medicine, Vol. 8, 20, 26.09.2008.

Research output: Contribution to journalArticle

Carratu, P, Scoditti, C, Maniscalco, M, Seccia, T, Di Gioia, G, Gadaleta, F, Cardone, R, Dragonieri, S, Pierucci, P, Spanevello, A & Resta, O 2008, 'Exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in COPD with pulmonary hypertension', BMC Pulmonary Medicine, vol. 8, 20. https://doi.org/10.1186/1471-2466-8-20
Carratu, Pierluigi ; Scoditti, Cristina ; Maniscalco, Mauro ; Seccia, Teresa ; Di Gioia, Giuseppe ; Gadaleta, Felice ; Cardone, Rosa ; Dragonieri, Silvano ; 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. In: BMC Pulmonary Medicine. 2008 ; Vol. 8.
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abstract = "Background: 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. Methods: 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. Results: 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 FEV1{\%}, (r = -0.59, p = 0.043), and PaPs negatively correlated to PaO2 (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.",
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AU - Carratu, Pierluigi

AU - Scoditti, Cristina

AU - Maniscalco, Mauro

AU - Seccia, Teresa

AU - Di Gioia, Giuseppe

AU - Gadaleta, Felice

AU - Cardone, Rosa

AU - Dragonieri, Silvano

AU - Pierucci, Paola

AU - Spanevello, Antonio

AU - Resta, Onofrio

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N2 - Background: 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. Methods: 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. Results: 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 FEV1%, (r = -0.59, p = 0.043), and PaPs negatively correlated to PaO2 (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.

AB - Background: 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. Methods: 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. Results: 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 FEV1%, (r = -0.59, p = 0.043), and PaPs negatively correlated to PaO2 (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.

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