Impairment of rat esophageal muscle contractility associated with experimental non‐erosive esophageal mucosal damage

New Findings

What is the central question of this study?

Is the responsiveness of isolated segments of the rat esophagus to contractile or relaxant stimuli susceptible to acute luminal exposure of the esophagus to an acid solution that contains pepsin and bile salt?

What is the main finding and its importance?

The study reveals that luminal acidity is an important factor that disrupts barrier function in the esophagus to allow the diffusion of noxious agents, such as bile acid, that alter the contractile status of the esophageal body, even in the absence of inflammation.

Abstract

The present study investigated whether the experimental simulation of duodeno‐gastro‐esophageal reflux alters the contractile responsiveness of rat esophageal strips. Following 30 min of luminal exposure to a solution at acid pH that contained pepsin and taurodeoxycholic acid (TDCA), isolated strips of the rat esophagus and gastroesophageal junction were subjected to contractile or relaxing stimuli. Acid challenge decreased the responsiveness of esophagus strips to contractile stimulation, especially in esophageal preparations that were mounted following the circular orientation of the muscularis externa layer. The contractility of longitudinal preparations of the rat esophagus appeared less susceptible to the deleterious effects of acid challenge. In contrast, the responsiveness of ring‐like preparations from the gastroesophageal junction to contractile stimulation was unaltered by acid challenge. TDCA decreased the responsiveness of circular esophageal preparations to KCl, an effect that was exacerbated by luminal acidity. Contrarily, whereas the relaxant ability of the rat esophagus did not change, acid challenge increased the relaxant efficacy of sodium nitroprusside and isoproterenol in strips of the gastroesophageal junction. A significant decrease in transepithelial electrical resistance (TEER) was seen when the esophageal mucosa was challenged at pH 1 but not at pH 4. Treatment with alginate blunted the deleterious effects of acid challenge on TEER and the responsiveness of esophageal preparations to KCl. The present findings support the notion that luminal acidity is an important factor that disrupts barrier function in the esophagus to allow the diffusion of noxious agents, such as bile acid, that alter the contractile status of the esophagus.

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