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Gastroesophageal reflux-induced bronchoconstriction. Is microaspiration a factor?
S M Harding1, C A Schan, M R Guzzo
1Division of Pulmonary and Critical Care Medicine, University of Alabama, Birmingham 35294, USA.
Chest
|November 1, 1995
Summary
Microaspiration does not significantly contribute to bronchoconstriction caused by gastroesophageal reflux. Acid reflux in asthmatics worsened airway resistance, but this was not linked to microaspiration.
Area of Science:
- Gastroenterology
- Pulmonology
- Clinical Medicine
Background:
- Gastroesophageal reflux disease (GERD) is a common condition.
- GERD can trigger bronchoconstriction in asthmatic patients.
- The exact mechanism of GERD-induced bronchoconstriction is not fully understood, with microaspiration being a potential factor.
Purpose of the Study:
- To investigate the role of microaspiration in gastroesophageal reflux-induced bronchoconstriction.
- To determine if proximal esophageal acid exposure correlates with changes in pulmonary function.
Main Methods:
- A prospective, blinded study was conducted with 30 participants (20 asthmatics with reflux, 10 with reflux only).
- Esophageal acid (0.1N HCl) and saline infusions were administered in a supine position.
- Pulmonary function tests, including spirometry and specific airway resistance (SRaw), were performed.
- Proximal esophageal acid exposure was monitored using a dual esophageal pH probe.
Main Results:
- Esophageal acid infusion led to decreased peak expiratory flow rate (PEF) and increased SRaw in the asthmatics with reflux group.
- These pulmonary function changes persisted despite acid clearance and were not associated with proximal esophageal acid exposure.
- SRaw continued to worsen during the recovery phase in the asthmatics with reflux group, suggesting a delayed effect.
Conclusions:
- Gastroesophageal acid reflux can induce bronchoconstriction in asthmatic individuals.
- The observed bronchoconstriction is not dependent on microaspiration or proximal esophageal acid exposure.
- A delayed bronchoconstrictor effect may be involved in the pathophysiology of GERD-induced asthma exacerbations.