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 language | English |
|---|---|
| Article number | 20 |
| Journal | BMC Pulmonary Medicine |
| Volume | 8 |
| DOIs | |
| Publication status | Published - Sep 26 2008 |
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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 journal › Article
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TY - JOUR
T1 - Exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in COPD with pulmonary hypertension
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
PY - 2008/9/26
Y1 - 2008/9/26
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.
UR - http://www.scopus.com/inward/record.url?scp=53949117573&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=53949117573&partnerID=8YFLogxK
U2 - 10.1186/1471-2466-8-20
DO - 10.1186/1471-2466-8-20
M3 - Article
C2 - 18822124
AN - SCOPUS:53949117573
VL - 8
JO - BMC Pulmonary Medicine
JF - BMC Pulmonary Medicine
SN - 1471-2466
M1 - 20
ER -