title: [Evidence of increased endogenous carbon monoxide production in asthma].
abstract: OBJECTIVE
  To investigate the role of carbon monoxide (CO) in the pathogenesis of asthma.
  
  
  METHODS
  We examined CO, nitrite and nitrate (NO2[not readable: see text]/NO3[not readable: see text]) and tumor necrosis factor alpha (TNF-alpha) levels in plasma of 26 asthmatic children and 22 matched normal children. At the same time, we examined the plasma and bronchoalveolar lavage fluid (BALF) CO, NO2[not readable: see text]/NO3[not readable: see text] and TNF-alpha levels in guinea-pigs with allergic asthma.
  
  
  RESULTS
  Asthmatic children in acute attack stage had increased levels of CO, NO2[not readable: see text]/NO3[not readable: see text] and TNF-alpha in plasma compared with normal control subjects (all P < 0.01), while in stable stage plasma CO and NO2[not readable: see text]/NO3[not readable: see text] reduced to normal levels (both of the P > 0.05), but TNF-alpha was still higher than the normal controls (P < 0.01). Guinea-pigs with allergic asthma had increased amounts of CO and TNF-alpha in plasma and CO, NO2[not readable: see text]/NO3[not readable: see text] and TNF-alpha in BALF as compared with normal control subjects (P < 0.05-0.01), but no changes in levels of circulating NO2[not readable: see text]/NO3[not readable: see text] (P > 0.05) were found. There was no difference between glucocorticoid treated asthmatic guinea pigs and normal controls in levels of CO, NO2[not readable: see text]/NO3[not readable: see text], and TNF-alpha. The elevation of plasma CO correlated with elevated NO2[not readable: see text]/NO3[not readable: see text] level in asthmatic children (P < 0.05), so did in the BALF in allergic guinea-pigs.
  
  
  CONCLUSIONS
  Our present data showed that endogenously produced CO was increased during the course of asthma, which suggested that the role of CO in asthma might worth further study.
authors.affiliation: Institute of Surgery, Daping Hospital, Third Military Medical University of PLA, Chongqing 400042.
authors.forename: D
authors.initials: D
authors.lastname: Jiang
authors.forename: Y
authors.initials: Y
authors.lastname: Shi
authors.forename: H
authors.initials: H
authors.lastname: Li
mesh_terms: D000818:Animals; D001249:Asthma / Q000209:etiology / Q000378:metabolism*; D001992:Bronchoalveolar Lavage Fluid; D002248:Carbon Monoxide / Q000378:metabolism*; D002460:Cell Line; D002648:Child; D002675:Child, Preschool; D004195:Disease Models, Animal; D005260:Female; D006168:Guinea Pigs; D006801:Humans; D007223:Infant; D008297:Male; D051379:Mice; D009566:Nitrates / Q000097:blood; D009573:Nitrites / Q000097:blood; D009585:Nitrogen Dioxide; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D009566:Nitrates; D009573:Nitrites; D014409:Tumor Necrosis Factor-alpha; D002248:Carbon Monoxide; D009585:Nitrogen Dioxide