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1 Division of Pediatric Gastroenterology, University of California, San Diego, San Diego, CA, USA; Division of Gastroenterology, VA Medical Center, San Diego, CA, USA
2 Division of Gastroenterology, VA Medical Center, San Diego, CA, USA
3 Division of Gastroenterology, University of California, San Diego, San Diego, CA, USA; Division of Gastroenterology, VA Medical Center, San Diego, CA, USA
* To whom correspondence should be addressed. E-mail: rmittal{at}ucsd.edu.
INTRODUCTION: Increase in intraesophageal pressure during transient lower esophageal sphincter relaxation (referred to as common cavity (CC) pressure) is thought to be a marker of gastroesophageal reflux (GER). Multi-luminal Impedance (MII) measurement is a sensitive marker of bolus entry into the esophagus during GER. We recorded GER using esophageal pressure, pH, impedance and intraluminal ultrasound (US) images to understand the genesis of the esophageal CC pressure. METHODS: 9 normal subjects underwent simultaneous MII/pH/pressure and US image recording of the esophagus for 2 hours following a standardized meal. MII and pressure transducers were located at 5 and 15 cm above the LES. The ultrasound transducer and pH sensors were also placed at 5 cm above the LES. Refluxate entry into the esophagus by MII criteria was determined relative to the onset of CC pressure wave. Esophageal lumen cross-sectional area (CSA) and muscle CSA during GER were determined from the US images. RESULTS: Eighty liquid GER episodes were identified using MII criteria of which 55 that were clearly associated with CC pressure wave were analyzed. The GER reached 15 cm above LES in 49/55 (89%) by MII criteria but CC pressure wave was observed at 5 and 15 cm during all episodes. The propagation of CC pressure wave was simultaneous at 5 and 15 cm during 49/55 (89%) of the GER episodes but the bolus entry by MII criteria was retrograde during 53/55 (96%) of these episodes. During 5 air reflux episodes, MII showed a simultaneous bolus entry between 5 and 15 cm site, however the CC pressure preceded bolus entry during all of these episodes. There was poor correlation between luminal CSA and magnitude of CC pressure (R2 = 0.144). US images revealed a close temporal correlation between CC pressure and increase in esophageal muscle thickness and muscle CSA (markers of longitudinal muscle contraction). CONCLUSIONS: Disassociation between CC pressure and MII detected reflux suggests that the onset of CC pressure is not due to GER. We speculate that longitudinal muscle contraction plays an important role in the genesis of CC pressure.
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