• Ratnawati Centre for Infection and Inflammation Research, School of Medical Sciences, University of New South Wales, New South Wales, Australia., John Morton, Richard L Henry, and Paul S Thomas.
• Centre for Infection and Inflammation Research, School of Medical Sciences, University of New South Wales, New South Wales, Australia.
• J Asthma. 2009 Dec 1; 46 (10): 1045-51.

BackgroundAirway narrowing after hypertonic saline challenge (HSC) is postulated to be mediated by bronchoconstrictors and inflammatory mediators.ObjectiveTo study the mechanism of this challenge by using exhaled breath condensate (EBC).MethodsFifty-six subjects (9 to 72 years of age) performed an HSC, with EBC collection and exhaled nitric oxide (FENO) measurements before and after the challenge. Bronchial hyper-reactivity (BHR) was defined if forced expiratory volume in 1 second (FEV1) decreased by 10% compared with baseline (PD10). EBC volume was recorded and was analyzed for mucin, histamine, nitrite/nitrate, and pH.ResultsThose with BHR had a significant rise in EBC volume/5-minute collection period after challenge (286.3 +/- 25.6 microl vs 402.2 +/- 31.3 microl, p = 0.0002), while BHR(-) subjects did not show this change (387.6 +/- 29.7 microl vs 364.1 +/- 30.1 microl, p = 0.55). FENO showed a significant decrease in both BHR(+) and BHR(-) groups after challenge (p = < 0.0001). In BHR(+) subjects histamine increased significantly (1.3 +/- 0.1 microM vs 1.5 +/- 0.1 microM, p = 0.006) compared with baseline, while EBC pH and mucin increased significantly after HSC in both groups. EBC nitrite did not change in either group.ConclusionEBC analysis suggests that HSC causes an increase in pH and mucin in both groups, but EBC volume and histamine only increased in the BHR(+) group. This suggests that mast cells are activated and fluid flux is associated with the positive response, while mucin release is independent of BHR in HSC.

44 keywords...

hide…