EFFECT OF ATROPINE ON ACUTE ANTIGEN-MEDIATED AIRWAY CONSTRICTION IN SUBJECTS WITH ALLERGIC-ASTHMA

Abstract

Exposure to antigen by inhalation challenge may produce airway constriction in patients with allergic asthma. To examine the role of reflex bronchoconstriction mediated by the vagus nerve in the antigen-induced airway response, the responses of 6 asthmatic volunteers were compared to inhaled ragweed antigen alone and to antigen given after pretreatment with atropine sulfate, a parasympathetic blocking agent. Significant increases in airway resistance were found, along with limitation of forced expiratory flow, increases in lung volumes and alterations in the distribution of inspired gas after antigen was given. When subjects were pretreated with atropine, a mean increase in the 1 s forced expired volume of 0.380 l (P < 0.025) and a mean increase in specific airway conductance of 0.067/s per cm H2O (P < 0.005) were observed. Atropine pretreatment did not prevent the responses to antigen in these subjects. After atropine pretreatment subjects began the antigen challenge with better pulmonary function and at a given antigen dose maintained a better level of function compared to when antigen was given alone. Differences in the absolute level of pulmonary function between the 2 challenges became smaller with the administration of larger antigen doses. Reflex bronchospasm involving postganglionic efferent parasympathetic nerve pathways is probably not a major component of the response to inhaled antigen in human allergic asthma.