Possible interaction between exposure to environmental tobacco smoke and therapy in children with asthma

1998 ◽  
Vol 95 (2) ◽  
pp. 143-149 ◽  
Author(s):  
Jean-Christophe DUBUS ◽  
Christiane ODDOZE ◽  
Monique BADIER ◽  
Chantal GUILLOT ◽  
Bernard BRUGUEROLLE

1.The aim of the study was to determine the carbachol and albuterol responsiveness in treated and untreated asthmatic and allergic children exposed to environmental tobacco smoke assessed by urinary cotinine measurements. 2.Forty-six asthmatic and allergic children with normal spirometric values were recruited. The doubling dose, concentration of carbachol producing a 2-fold increase in specific airway resistance (SRaw) was determined and 200 ;μg of albuterol were administered via a Volumatic® spacer. The percentage of bronchodilatation was defined as the difference between the largest obtained SRaw and the post-β2 SRaw divided by the largest SRaw. Data were compared by a Mann–Whitney U-test. 3.The 23 children with a high urinary cotinine, compared with the 23 children without urinary cotinine, had a decreased doubling dose (108.2±14.7 ;μg versus 160.9±19.5 ;μg; P = 0.04) and an increased percentage of bronchodilatation (74.8±1.4% versus 68.8±1.8%; P = 0.03). A prophylactic anti-inflammatory treatment induced a weaker bronchial reactivity to carbachol and a slightly greater bronchodilatation in children exposed to environmental tobacco smoke. 4.Environmental tobacco smoke increases bronchial reactivity in asthmatic and allergic children. This effect might be reduced by anti-inflammatory therapy. The bronchodilator response may be enhanced in exposed children and may be caused by one or several direct interactions between tobacco smoke compounds and albuterol.

2008 ◽  
Vol 8 (5) ◽  
pp. 288-293 ◽  
Author(s):  
Maria Fagnano ◽  
Kelly M. Conn ◽  
Jill S. Halterman

1990 ◽  
Vol 79 (4) ◽  
pp. 325-330 ◽  
Author(s):  
Alan J. Knox ◽  
John R. Britton ◽  
Anne E. Tattersfield

1. We have recently shown that ouabain, an inhibitor of Na+/K+-adenosine triphosphatase, causes contraction of bovine and human airways in vitro, and that amiloride causes relaxation and inhibits receptor-operated contraction in bovine trachealis. 2. To determine whether such drugs alter bronchial reactivity in vivo, we have studied the effect of oral digoxin (an inhibitor of Na+/K+-adenosine triphosphatase) and oral and inhaled amiloride on bronchial reactivity to histamine in three double-blind, placebo-controlled studies. 3. Histamine reactivity was measured as the provocative dose causing a 20% reduction in the forced expiratory volume in 1 s (PD20FEV1) or, when normal subjects were included, the provocative dose causing a 35% reduction in the specific airways conductance (PD35sGaw); the results are given as geometric mean values. 4. In study 1, 13 atopic asthmatic subjects were given 20 mg of oral amiloride or placebo on separate days. Two hours after the drug, the geometric mean PD20FEV1 for histamine was 0.43 μmol after amiloride and 0.54 μmol after placebo (95% confidence intervals for the difference: 0.9 to −0.2 doubling doses of histamine; P = 0.2). 5. In study 2, six normal and 24 atopic asthmatic men inhaled 10 ml of 10−2 mol/l amiloride or diluent control in a crossover study. The mean values of PD35sGaw for histamine immediately after inhalation of amiloride and placebo were 3.0 μmol and 4.3 μmol, respectively, in the normal subjects (95% confidence intervals for the difference: −0.53 to 1.52 doubling doses, P = 0.2), and 0.33 μmol and 0.29 μmol in the asthmatic subjects (95% confidence intervals for the difference: −0.95 to 0.57 doubling doses; P = 0.6). 6. In study 3, 24 atopic asthmatic men were treated for 7 days with placebo or oral digoxin (1.5 mg loading dose plus 0.25 mg twice daily for 6 days). The PD20FEV1 for histamine was measured before, 12 h after the loading dose and on day 7 of treatment. The change in PD20FEV1 did not differ significantly after digoxin and placebo, after either 1 day's treatment [mean (95% confidence intervals) difference: 0.56 doubling dose (−0.37 to 1.5 doubling dose)] or 7 day's treatment [mean (95% confidence intervals) difference: 0.3 doubling dose (−1.23 to 1.8 doubling doses)]. 7. Although our work in vitro has suggested that membrane sodium transport may play an important role in determining airway smooth muscle contractility, we have been unable to demonstrate any effect of the sodium-transport inhibitors amiloride and digoxin on histamine reactivity in these studies.


CHEST Journal ◽  
2001 ◽  
Vol 120 (5) ◽  
pp. 1709-1722 ◽  
Author(s):  
Sandra R. Wilson ◽  
Eileen G. Yamada ◽  
Reddivalam Sudhakar ◽  
Lauro Roberto ◽  
David Mannino ◽  
...  

1998 ◽  
Vol 95 (2) ◽  
pp. 143 ◽  
Author(s):  
Jean-Christophe DUBUS ◽  
Christiane ODDOZE ◽  
Monique BADIER ◽  
Chantal GUILLOT ◽  
Bernard BRUGUEROLLE

2009 ◽  
Vol 19 (2) ◽  
pp. 97-108 ◽  
Author(s):  
Akira Yamasaki ◽  
Keichi Hanaki ◽  
Katsuyuki Tomita ◽  
Masanari Watanabe ◽  
Yasuyuki Hasagawa ◽  
...  

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