In a double-blind, randomized, placebo-controlled, two-way crossover study, salbutamol significantly lowered mannitol-induced coughing in allergic asthmatic and healthy participants. The absence of airway caliber changes in healthy individuals suggests salbutamol may exert effects beyond its known bronchodilatory role.
The study included 20 mild, steroid-naïve allergic asthmatic patients and 20 healthy controls. Participants were matched for age, sex, and baseline lung function. The maximum number of coughs (Emax) evoked by mannitol was measured after administration of either salbutamol or placebo. Mannitol-evoked cough dose ratio (CDR) was significantly lower in healthy controls than in asthmatics (5.63 ± 1.84 vs 7.32 ± 3.67 coughs; p = 0.023). However, both groups showed similar values for Emax, C2 (dose causing two coughs), and C5 (dose causing five coughs) under baseline conditions.
In allergic asthmatics, mannitol decreased forced expiratory volume in one second (FEV1) by 8.11 ± 2.32% with placebo, significantly attenuating to 3.19 ± 1.16% with salbutamol (p = 0.03). In healthy controls, FEV1 reduction following mannitol was not significant. Emax in asthmatics decreased from 8.90 (8.09–9.80) coughs with placebo to 7.07 (6.28–8.00) with salbutamol (p < 0.001). In healthy controls, Emax dropped from 8.19 (7.08–9.61) coughs with placebo to 4.95 (4.38–5.66) with salbutamol (p < 0.001). The between-group difference in Emax response to salbutamol was also statistically significant (p < 0.001).
In allergic asthmatics, salbutamol significantly improved CDR, C2, and C5 values (p < 0.05), although no significant differences were seen between groups for these parameters. The findings indicate that salbutamol reduces mannitol-evoked coughs in both groups. This effect was independent of FEV1 changes in healthy individuals, suggesting mechanisms beyond airway smooth muscle relaxation.
