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. 2011 Feb;120(2):137-42.
doi: 10.1177/000348941112000211.

Response of cricopharyngeus muscle to esophageal stimulation by mechanical distension and acid and bile perfusion

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Response of cricopharyngeus muscle to esophageal stimulation by mechanical distension and acid and bile perfusion

Natalya Chernichenko et al. Ann Otol Rhinol Laryngol. 2011 Feb.

Abstract

Objectives: The aim of this study was to identify the response of the cricopharyngeus muscle (CPM) to esophageal stimulation by intraluminal mechanical distension and intraluminal acid and bile perfusion.

Methods: In 3 adult pigs, electromyographic (EMG) activity of the CPM was recorded at baseline and after esophageal stimulation at 3 levels: proximal, middle, and distal. The esophagus was stimulated with 20-mL balloon distension and intraluminal perfusion of 40 mL 0.1N hydrochloric acid, taurocholic acid (pH 1.5), and chenodeoxycholic acid (pH 7.4) at the rate of 40 mL/min. The EMG spike density was defined as peak-to-peak spikes greater than 10 microV averaged over 10-ms intervals.

Results: In all 3 animals, the spike density at baseline was 0. The spike densities increased after proximal and middle distensions to 15.2 +/- 1.5 and 5.1 +/- 1.2 spikes per 10 ms, respectively. No change in CPM EMG activity occurred after distal distension. The spike density following intraluminal perfusion with hydrochloric acid at the distal level was 10.1 +/- 1.1 spikes per 10 ms. No significant change in CPM EMG activity occurred after acid perfusion at the middle and proximal levels. No change in CPM EMG activity occurred after intraluminal esophageal perfusion with either taurocholic acid or chenodeoxycholic acid.

Conclusions: Proximal esophageal distension, as well as distal intraluminal acid perfusion, appeared to be important mechanisms in generation of CPM activity. Bile acids, on the other hand, failed to evoke such CPM activity. The data suggest that transpyloric refluxate may not be significant enough to evoke the CPM protective sphincteric function, thereby placing supraesophageal structures at risk of bile injury.

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