Study objective: To evaluate the role of microaspiration in gastroesop
hageal reflux-induced bronchoconstriction. Design: Prospective study b
linded to the subject. Setting: Outpatient laboratory of a 908-bed uni
versity hospital. Participants: Thirty nonsmoking adults divided into
two groups: asthmatics with reflux (AR), 20; and subjects with gastroe
sophageal reflux (R), 10. Interventions: Dual esophageal pH probe plac
ed. Esophageal infusions of normal saline solution, 0.1N hydrochloric
acid, then normal saline solution, each lasting 18 min, were followed
by two 20-min recovery periods. Subjects remained in the supine positi
on throughout. Spirometry and specific airway resistance (SRaw) perfor
med at baseline, after each esophageal infusion and recovery period. P
roximal esophageal acid exposure, a requirement for microaspiration, w
as assessed by the proximal esophageal pH probe. Results: Peak expirat
ory flow rate (PEF) decreased with esophageal acid in the AR group and
did not recover immediately despite esophageal acid clearance with a
significant main effect of subject groups (p<0.021) by repeated measur
es analysis of covariance. This decrease in PEF was not associated wit
h the presence of proximal esophageal acid exposure (p=0.618). Specifi
c airway resistance increased in the AR group with esophageal acid and
worsened despite acid clearance, especially during the second recover
y phase, with a significant phase (p<0.009) and group by treatment eff
ect (p<0.009). The presence of proximal esophageal acid exposure was n
ot associated with this deterioration in SRaw (p=1.0). Conclusions: Es
ophageal acid infusions given in the supine position caused a decrease
in PEF and an increase in SRaw in the asthma with reflux group, which
did not improve despite acid clearance. These responses were not depe
ndent on proximal esophageal acid exposure. Also, SRaw continued to wo
rsen during the recovery phase in the AR group, which may represent a
delayed bronchoconstrictor effect. These data suggest thai microaspira
tion does not play significant role in esophageal acid-induced broncho
constriction.