Rectal distention increases the frequency and duration of transient lower esophageal sphincter relaxations in anesthetized dogs– a putative rectoesophageal reflex

Jose Ronaldo Vasconcelos Graça,Jose Ricardo Cunha Neves,Willy Okoba,Sidney Wendell Goiana Da Silva

doi:10.20513/2447-6595.2019v59n3p24-31

Jose Ronaldo Vasconcelos Graça, Jose Ricardo Cunha Neves + Show 2 more

Open Access

https://doi.org/10.20513/2447-6595.2019v59n3p24-31

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Abstract

Introduction: The esophagus is subject to frequent reflux of gastric contents as a normal phenomenon during episodes of transient lower esophageal sphincter relaxation (tLESR), responsible too, for pathologic reflux. However, pathologic reflux is mostly associated with reflux of acid contents. Distending the stomach provokes an increase in frequency of tLESR. Objective: To investigate the effect of distending the rectum on the tLESR and possible involved pathways. Methods: Forty four (Protocol: 096/07) street dogs were selected and divided into respective protocols: Rectal distention (RD), Gastric distention (GD), RD+GD, Atropine+RD, Hexamethonium+RD, Baclofen+RD, Bilateral Pudendal nerve section+RD and Spinal cord transection+RD. We determined and compared the tLESR of each group and subjected data to statistical analysis. Values of p<0.05 were regarded as statistically significant. Results: RD provoked a significant increase in the tLESR just as GD, with RD+GD provoking the highest value of tLESR. This increase in tLESR due to RD was prevented in A+RD, B+RD, Bilateral Pudendal nerve section+RD and Spinal cord transection+RD but not Hexamethonium+RD protocols. Conclusion: RD is a significant inducer of an increase in tLESR with participation of muscharinic and GABAβ, sensitive and spinal cord neurons, but not nicotinic receptors.

Highlights

The esophagus is subject to frequent reflux of gastric contents as a normal phenomenon during episodes of transient lower esophageal sphincter relaxation, responsible too, for pathologic reflux
Our results showed that like gastric distention (GD), rectal distention (RD) provoked a significant increase in the frequency of transient lower esophageal sphincter relaxation (tLESR), without evoking changes in gastric or lower esophageal sphincter (LES) pressure
Rectal distention combined with gastric distention (RD+GD) evoked the highest increase in the frequency of tLESR, but provoked similar results on the latency and duration of tLSER-episode, just as either GD or RD

Summary

Introduction

The esophagus is subject to frequent reflux of gastric contents as a normal phenomenon during episodes of transient lower esophageal sphincter relaxation (tLESR), responsible too, for pathologic reflux. Results: RD provoked a significant increase in the tLESR just as GD, with RD+GD provoking the highest value of tLESR This increase in tLESR due to RD was prevented in A+RD, B+RD, Bilateral Pudendal nerve section+RD and Spinal cord transection+RD but not Hexamethonium+RD protocols. The major stimulus for tLESR is the post-prandial gastric distention, via activation of a reflex pathway involving mechanoreceptors located in the subcardial area, vagal afferents, nucleus of the tractus solitarius (NTS) in the brainstem, as well as inhibitory efferents to the LES.[3] In addition to this inhibitory reflex, other inhibitory reflexes originating from the small intestine or the colons influence the behaviour of the esophago-gastric junction, either directly or by modulating gastric tonus.[4,5] For instance, healthy individuals subjected to voluntary obstipation present a gastric emptying delay of test meals.[6] In addition, a revision of literature shows that the prevalence of GERD symptoms in patients with inflammatory bowel disease is approximately

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