Effect of atropine on experimentally-induced airway obstruction in man.

The effect of pretreatment with inhaled atropine methonitrate 1.5 mg and placebo was compared on standardized inhalation challenges with histamine acid phosphate in normal and asthmatic subjects and with antigen in atopic asthmatics. The response was monitored with measurements of specific airway conductance (sGaw). Challenges were repeated, as often as necessary, to obtain responses whose baseline sGaw after premedication varied by less than 35% within an individual. The anticholinergic effect of atropine 1.5 mg was studied on the methacholine response in all subjects. Atropine inhibited the methacholine response and, therefore, the dose was judged adequate to produce cholinergic blockade in the airways. Similar degrees of bronchodilatation (47-49% increase in sGaw) were found in normal subjects and in non-atopic asthmatics, but greater bronchodilatation was achieved in atopic asthmatics (100% increase in sGaw). Among the asthmatics, the lower the initial sGaw the greater the bronchodilatation with atropine. When prechallenge bronchial tone was comparable within individuals, atropine inhibited the mean histamine response of both normal and asthmatic groups and inhibited the mean antigen response of the atopic asthmatics, whereas placebo had no significant effect. No correlation was found between post-atropine sGaw and the effect of atropine on either histamine or antigen response. In conclusion, atropine is a powerful bronchodilator, particularly in atopic asthmatics with increased bronchomotor tone. Histamine- and antigen-induced bronchoconstriction is inhibited by atropine, but the extent of this inhibition varies between subjects.U