![]() Q aw is an expression of bronchial blood flow, whereas Δe°T reflects the rate of temperature increase in the exhaled breath. To test this, we investigate the relationship between airway inflammation as assessed by exhaled NO, with Q aw and Δe°T measured non-invasively. In the present study we hypothesise that elevated Δe°T may result from increased heat exchange in the airways due to elevated bronchial blood flow (Q aw) caused by inflammation and airway remodelling. and that this may be due to airway inflammation and elevated levels of NO. Therefore, we suggested that patients with asthma have high Δe°T. In a recent study we have found that patients with asthma have higher increases of exhaled breath temperature (Δe°T) compared with normal subjects and that this is correlated to the concentration of exhaled nitric oxide (NO). The increased vascularity of the airways in asthma is partly due to the elevated number of vessels associated with angiogenesis and partly due to vasodilation caused by the release of vasodilator mediators, such as, histamine, bradykinin, and nitric oxide (NO). Vasodilatation is a critical feature of inflammation, and angiogenesis and vascular remodelling are features of chronic inflammatory diseases, such as asthma. Δe°T correlates with Q aw and exhaled NO in asthmatic patients and therefore may reflect airway inflammation, as confirmed by the rapid response to steroids.Īsthma is an inflammatory disease of the airways. In asthma patients, Q aw was reduced 30 minutes after the inhalation of budesonide 400 μg (21.0 ± 2.3 μl/ml/min, p < 0.05) but was not affected by salbutamol. Q aw, measured using an acetylene dilution method was also elevated in patients with asthma compared to normal subjects (49.47 ± 2.06 and 31.56 ± 1.6 μl/ml/min p < 0.01) and correlated with exhaled NO (r = 0.57, p < 0.05) and Δe°T (r = 0.525, p < 0.05). Δe°T was confirmed to be elevated (7.27 ± 0.6 Δ☌/s) in 19 asthmatic subjects (mean age ± SEM, 40 ± 6 yr 6 male, FEV 1 74 ± 6 % predicted) compared to 16 normal volunteers (4.23 ± 0.41 Δ☌/s, p < 0.01) (30 ± 2 yr) and was significantly increased after salbutamol inhalation in normal subjects (7.8 ± 0.6 Δ☌/ s, p < 0.05) but not in asthmatic patients. We also studied the anti-inflammatory and vasoactive effects of inhaled corticosteroid and β 2-agonist. ![]() ![]() We investigated the relationship of Δe°T with Q aw and airway inflammation as assessed by exhaled nitric oxide (NO). In asthma elevated rates of exhaled breath temperature changes (Δe°T) and bronchial blood flow (Q aw) may be due to increased vascularity of the airway mucosa as a result of inflammation. ![]()
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