title: [Endogenous hydrogen sulfide in patients with chronic obstructive pulmonary disease].
abstract: OBJECTIVE
  To investigate the role of endogenous hydrogen sulfide (H(2)S) in patients with chronic obstructive pulmonary disease (COPD).
  
  
  METHODS
  Levels of serum H(2)S and nitric oxide (NO), lung function and cell differential count in induced sputum were studied in 27 patients with acute exacerbation of COPD (AECOPD), 37 patients with stable COPD and 13 health subjects. Echo-Doppler assessment and arterial blood gas were measured in patients with AECOPD.
  
  
  RESULTS
  (1) The serum H(2)S level was significantly higher in patients with stable COPD [(50.8 +/- 2.5) micromol/L] as compared to those in the controls [(39.8 +/- 1.6) micromol/L] and in patients with AECOPD [(33.5 +/- 2.2) micromol/L, P < 0.01]. (2) The level of serum H(2)S was significantly lower in smokers with AECOPD [(28.1 +/- 1.3) micromol/L] as compared to nonsmokers with AECOPD [(39.4 +/- 3.9) micromol/L, P < 0.05] and healthy nonsmokers [(39.8 +/- 1.6) micromol/L, P < 0.01]. (3) There was significant difference in the serum H(2)S level among stable COPD patients with different severity of airway obstruction (P < 0.05); being lower in patients with stage III [(45.1 +/- 4.1) micromol/L] as compared to stage I obstruction [(70.2 +/- 6.2) micromol/L, P < 0.05]. (4) AECOPD with pulmonary hypertension pulmonary artery systolic pressure (PASP) > or = 35 mm Hg (1 mm Hg = 0.133 kPa) showed a lower serum H(2)S level [(26.3 +/- 2.2), (36.2 +/- 2.5) micromol/L, P < 0.05] than that with a normal resting PASP. (5) H(2)S in serum was positively correlated with NO levels (r = 0.278, P = 0.029), FEV(1)% predicted values (r = 0.533, P = 0.000), percentage of sputum lymphocytes (r = 0.286, P = 0.028) and macrophages (r = 0.334, P = 0.01); and negatively correlated with PASP (r = -0.561, P = 0.011) and the percentage of sputum neutrophils (r = -0.422, P = 0.001) in patients with COPD.
  
  
  CONCLUSIONS
  Endogenous H(2)S may be involved in the pathogenesis of airway obstruction in COPD and may be a noninvasive marker of disease activity and severity.
authors.affiliation: Department of Respiratory Medicine, Peking University Third Hospital, Beijing 100083, China.
authors.forename: Ya-hong
authors.initials: YH
authors.lastname: Chen
authors.forename: Wan-zhen
authors.initials: WZ
authors.lastname: Yao
authors.forename: Bin
authors.initials: B
authors.lastname: Geng
authors.forename: Yan-ling
authors.initials: YL
authors.lastname: Ding
authors.forename: Ming
authors.initials: M
authors.lastname: Lu
authors.forename: Ming-wu
authors.initials: MW
authors.lastname: Zhao
authors.forename: Chao-shu
authors.initials: CS
authors.lastname: Tang
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D006862:Hydrogen Sulfide / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000097:blood; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology*; D044967:Serum / Q000737:chemistry
chemical_list: D009569:Nitric Oxide; D006862:Hydrogen Sulfide