Intraesophageal Perfusion of Acid Increases the Bronchomotor Response to Methacholine and to Isocapnic Hyperventilation in Asthmatic Subjects1–3

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Abstract
Gastroesophageal reflux (GER) has been shown to be more frequent in people with asthma, but the mechanism by which it might aggravate asthmatic symptoms remains unclear. We compared the effects on maximal expiratory flow at 50% of VC (MEF50) of esophageal perfusion of hydrochloric acid (HCl) and of normal saline (NaCl) in 12 asthmatic subjects chosen at random. In all subjects, HCl perfusion did not change MEF50 but potentiated the bronchoconstriction induced by isocapnic hyperventilation of dry air (maximal decrease in MEF50 = 44 ± 7% with HCl versus 22 ± 5% with NaCl; p < 0.001) or methacholine (provocative dose producing a 20% decrease in FEV1 = 349 ± 99 µg with HCl versus 496 ± 119 µg with NaCl; p < 0.01). Seven of the asthmatic subjects were found to have GER on esophageal pH monitoring. In these subjects, HCl alone decreased MEF50 slightly but significantly (−17.5 ± 5.5%; p < 0.05), possibly reflecting the higher degree of basal bronchial hyperreactivity observed in this group. Thus, perfusion of acid into the distal esophagus caused slight but significant bronchoconstriction in asthmatic subjects with GER and increased the bronchoconstriction produced by isocapnic hyperventilation and by methacholine in asthmatic subjects without regard for the presence of GER.

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