Abstract
peristalsis could be modulated by baclofen and mosapride. Methods: In all 15 healthy subjects (5 female, mean age 22, range 20-26 yr), secondary peristalsis was generated by slow and rapid mid-esophageal injections of air after a baseline recording of esophageal motility. Three separate sessions with 40 mg oral baclofen, 40 mg oral mosapride or placebo were randomly performed to test their effects on esophageal secondary peristalsis with at least a 1-week interval. Results: Baclofen significantly increased the threshold volume for triggering secondary peristalsis during slow air distension (P = 0.003) and rapid air distension (P = 0.002). Baclofen significantly reduced the rate of secondary peristalsis by rapid air distension from 90% to 30% (P = 0.0002). Despite increasing basal LES pressure (P = 0.03), baclofen did not affect any of peristaltic parameters by primary or secondary peristalsis. Mosapride significantly decreased the threshold volume for triggering secondary peristalsis during rapid air distension (P = 0.04). Secondary peristalsis was triggered more frequently in response to rapid air distension after application of mosapride (P = 0.02). Mosapride significantly increased pressure wave amplitudes of secondary peristalsis during slow (P = 0.001) and rapid air distension (P = 0.002). Conclusions: Inhibition of baclofen on the triggering of secondary peristalsis presents during esophageal distension, indicating that sensory part of secondary peristalsis is probably mediated by the GABAB receptors. However, baclofen does not lead to any motility change in secondary peristalsis as induced by either slow or rapid air distension. Mosapride appears to enhance sensitivity to distension-induced secondary peristalsis and facilitates secondary peristaltic contractility, suggesting the involvement of 5-HT4 in the modulation of esophageal secondary peristalsis in humans.
Published Version
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