The vasoconstrictive efficacies of glucocorticosteroids (GS) are usually compared by the McKenzie skin-blanching test and taken as an index of relative potency. The rationale for the present study was to transpose the McKenzie test to the airway and to compare the airway vascular effects of three inhaled GS: beclomethasone dipropionate (BDP), fluticasone propionate (FP) and budesonide (BUD), in healthy subjects and patients with mild stable asthma.A soluble, inert gas-uptake method was used to measure airway blood flow (Qaw). Baseline mean¡SD Qaw normalised for anatomical dead space was 53.1¡1.4 mL?minin healthy subjects (n=10) and 67.8¡3 mL?min -1 ?mL -1 in asthmatics (n=10). All GS caused a transient decrease in Qaw. The magnitude of the vasoconstriction was greater in asthmatics. The relative vasoconstrictive effect of BDP, FP and BUD was 1, 1.9, and 2.7, respectively, in asthmatics and 1, 3.3 and 3.0, respectively, in healthy subjects, as assessed by the dose required to decrease Qaw by 20% from the baseline, 30-min postdrug inhalation.Therefore, measuring airway blood flow may be a useful, site-specific parameter to assess the tissue bioavailability and vasoconstrictive efficacy of inhaled glucocorticosteroids. Eur Respir J 2003; 21: 989-993.

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Although the relative effect of racemic and (R)-albuterol on airway smooth muscle tone have been investigated in patients with airflow obstruction, the comparative effectiveness of these drugs in relaxing airway vascular smooth muscle is unknown. Therefore, we determined the actions of inhaled racemic and (R)-albuterol on airway mucosal blood flow (Qaw) normalized for anatomic dead space as an index of airway vascular smooth muscle tone in 11 healthy subjects and 10 subjects with mild asthma. We also monitored the forced expiratory volume in 1 second (FEV1) as an index of airway smooth muscle tone. Mean +/- SE baseline Qaw was 43.1 +/- 1.5 microl x min(-1) x ml(-1) in healthy subjects and 53.4 +/- 2.1 microl x min(-1) x ml(-1) in asthmatic subjects (p < 0.01). The corresponding values for FEV1 were 95.6 +/- 1.4 and 86.8 +/- 2.5% respectively, of predicted (p = 0.01). Racemic and (R)-albuterol caused a transient, dose-dependent increase of Qaw in healthy, but not in asthmatic subjects; the responses were not different between the two drugs. The FEV1 tended to increase more in asthmatics than in healthy subjects, again without a difference between the two drugs. These results show that racemic and (R)-albuterol have comparable effects on airway vascular smooth muscle and suggest that the blunted airway vascular smooth muscle response to albuterol in asthmatics is not related to (S)-albuterol.