title: Exhaled and arterial levels of endothelin-1 are increased and correlate with pulmonary systolic pressure in COPD with pulmonary hypertension.
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.
authors.affiliation: Institute of Pulmonary Disease, University of Bari, Italy. pierluigicarratu@yahoo.com
authors.forename: Pierluigi
authors.initials: P
authors.lastname: Carratu
authors.forename: Cristina
authors.initials: C
authors.lastname: Scoditti
authors.forename: Mauro
authors.initials: M
authors.lastname: Maniscalco
authors.forename: Teresa Maria
authors.initials: TM
authors.lastname: Seccia
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Di Gioia
authors.forename: Felice
authors.initials: F
authors.lastname: Gadaleta
authors.forename: Rosa Angela
authors.initials: RA
authors.lastname: Cardone
authors.forename: Silvano
authors.initials: S
authors.lastname: Dragonieri
authors.forename: Paola
authors.initials: P
authors.lastname: Pierucci
authors.forename: Antonio
authors.initials: A
authors.lastname: Spanevello
authors.forename: Onofrio
authors.initials: O
authors.lastname: Resta
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000378:metabolism; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000502:physiology*; D001944:Breath Tests; D016022:Case-Control Studies; D019332:Endothelin-1 / Q000378:metabolism*; D045853:Exhalation / Q000502:physiology; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D006976:Hypertension, Pulmonary / Q000378:metabolism* / Q000503:physiopathology; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D019332:Endothelin-1; D009569:Nitric Oxide