Research article

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

Pierluigi Carratu¹ , Cristina Scoditti¹ , Mauro Maniscalco² , Teresa Maria Seccia¹ , Giuseppe Di Gioia¹ , Felice Gadaleta¹ , Rosa Angela Cardone³ , Silvano Dragonieri¹ , Paola Pierucci¹ , Antonio Spanevello⁴ and Onofrio Resta¹

¹  Institute of Pulmonary Disease, University of Bari, Italy

²  Institute of Pulmonary Disease, University of Naples, Italy

³  Department of General and Environmental Physiology, University of Bari, Italy

⁴  Institute of Pulmonary Disease, University of Foggia, Italy

author email corresponding author email

BMC Pulmonary Medicine 2008, 8:20doi:10.1186/1471-2466-8-20

Published:	26 September 2008

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.