Mohammad Hossein Boskabady1, Hamed Farhadi. 1. Department of Physiology, Ghaem Medical Centre, Mashhad University of Medical Sciences, Mashhad, Iran. m-boskabady@mums.ac.ir
Abstract
BACKGROUND: Airway hyperresponsiveness (AHR), the most characteristic feature of asthma, is reported in COPD patients and smokers. There are controversies, however, regarding airway responsiveness to b-adrenergic agonists in asthma as well as COPD and smokers. After our previous studies had shown AHR to b-agonists in asthmatic patients, we examined airway responsiveness to salbutamol and its relationship to responsiveness to methachline in smokers. MATERIAL/ METHODS: The threshold concentrations of inhaled salbutamol or methacholine required for a 20% change in forced expiratory flow in 1 sec (FEV1), recorded as PC20, or a 35% change in specific airway conductance (sGaw), recorded as PC35, was measured in 14 nonsmoker and 14 smokers. RESULTS: Airway responsiveness to salbutamol was greater in smokers (PC20=66.85, PC35=22.74 mg/l) than in nonsmokers (PC20=241.42, PC35 =88.72 mg/l, p<0.001 for both). Airway responsiveness to methacholine was also significantly greater in smokers (PC20= 1.34 and PC(35)=1.01 g/l) than nonsmokers (PC20=5.66 and PC35=4.63 g/l, P<0.001 for both cases). There were significant correlations between FEV(1)with both PC20 salbutamol (r=0.577, p<0.001) and PC20 methacholine (r=0.638), (p<0.001 for both cases). The correlations between airway responsiveness to salbutamol with responsiveness to methacholine using both PC(20) (r=0.819) and PC(35) (r=0.783) were also statistically significant (p<0.001 for both cases). The slopes of the concentration-response curves of both agents were significantly greater in smokers than nonsmoker (P<0.001 for all cases). CONCLUSIONS: These results showed increased sensitivity of smokers' airways to salbutamol, which correlates closely to airway responsiveness to methacholine.
BACKGROUND:Airway hyperresponsiveness (AHR), the most characteristic feature of asthma, is reported in COPDpatients and smokers. There are controversies, however, regarding airway responsiveness to b-adrenergic agonists in asthma as well as COPD and smokers. After our previous studies had shown AHR to b-agonists in asthmatic patients, we examined airway responsiveness to salbutamol and its relationship to responsiveness to methachline in smokers. MATERIAL/ METHODS: The threshold concentrations of inhaled salbutamol or methacholine required for a 20% change in forced expiratory flow in 1 sec (FEV1), recorded as PC20, or a 35% change in specific airway conductance (sGaw), recorded as PC35, was measured in 14 nonsmoker and 14 smokers. RESULTS: Airway responsiveness to salbutamol was greater in smokers (PC20=66.85, PC35=22.74 mg/l) than in nonsmokers (PC20=241.42, PC35 =88.72 mg/l, p<0.001 for both). Airway responsiveness to methacholine was also significantly greater in smokers (PC20= 1.34 and PC(35)=1.01 g/l) than nonsmokers (PC20=5.66 and PC35=4.63 g/l, P<0.001 for both cases). There were significant correlations between FEV(1)with both PC20 salbutamol (r=0.577, p<0.001) and PC20 methacholine (r=0.638), (p<0.001 for both cases). The correlations between airway responsiveness to salbutamol with responsiveness to methacholine using both PC(20) (r=0.819) and PC(35) (r=0.783) were also statistically significant (p<0.001 for both cases). The slopes of the concentration-response curves of both agents were significantly greater in smokers than nonsmoker (P<0.001 for all cases). CONCLUSIONS: These results showed increased sensitivity of smokers' airways to salbutamol, which correlates closely to airway responsiveness to methacholine.