The effect of oxitropium bromide on neurokinin A-induced bronchoconstriction in asthmatic subjects.
In some animal species substance P and neurokinin A (NKA) cause bronchoconstriction by the release of acetylcholine from postganglionic cholinergic nerve endings. The aim of the present study was to investigate the effect of an anticholinergic drug, oxitropium bromide, on bronchoprovocation with NKA in asthmatics. Eleven mild asthmatics (mean % predicted FEV1 85.5) received on 2 separate days, double blind, in a randomised order, 400 mcg oxitropium bromide or placebo, 90 min before challenge with NKA. NKA was inhaled at 3 concentrations (10(-4), 3.10(-4) and 10(-3) M). Specific airways conductance (sGaw) and forced expiratory volume in 1 s (FEV1) were used as parameters of airway calibre. Compared to the placebo-aerosol, oxitropium bromide caused a significant increase in sGaw and FEV1. On the placebo-treatment day, NKA caused a concentration-dependent decrease in sGaw and FEV1. The percentage changes in sGaw and FEV1 on the oxitropium day were not statistically different from those occurring on the placebo day. We conclude that oxitropium bromide caused a significant bronchodilation but offered no significant protection against NKA-induced bronchoconstriction in mild asthmatic subjects.
Joos
G
G
University Hospital, Department of Respiratory Diseases, Ghent, Belgium.
Pauwels
R
R
Van Der Straeten
M
M
D000328:Adult; D001249:Asthma / Q000503:physiopathology*; D016084:Bronchoconstriction / Q000187:drug effects*; D005260:Female; D006801:Humans; D008297:Male; D015288:Neurokinin A / Q000494:pharmacology*; D010276:Parasympatholytics / Q000494:pharmacology*; D012602:Scopolamine Derivatives / Q000494:pharmacology*
D010276:Parasympatholytics; D012602:Scopolamine Derivatives; D015288:Neurokinin A; C017590:oxitropium