GASTROESOPHAGEAL REFLUX-INDUCED BRONCHOCONSTRICTION - IS MICROASPIRATION A FACTOR

Citation
Sm. Harding et al., GASTROESOPHAGEAL REFLUX-INDUCED BRONCHOCONSTRICTION - IS MICROASPIRATION A FACTOR, Chest, 108(5), 1995, pp. 1220-1227
Citations number
33
Categorie Soggetti
Respiratory System
Journal title
ChestACNP
ISSN journal
00123692
Volume
108
Issue
5
Year of publication
1995
Pages
1220 - 1227
Database
ISI
SICI code
0012-3692(1995)108:5<1220:GRB-IM>2.0.ZU;2-C
Abstract
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.