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

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.

Observational cohort study: Getting to the bottom of laryngopharyngeal reflux—It’s a motility disorder and not just about the acid

“…But physiological studies in IBS clearly demonstrate that colonic distension induces colonic discomfort and increases colonic contractility with IBS patients having a lower threshold vs controls . Colonic or rectal distension has also been shown to impair small intestinal transit, gastric emptying and oesophageal motility as well as increasing TLOSRs with associated reflux events . Past clinical studies have confirmed that patients presenting with refractory GORD and recurrent vomiting, functional dyspepsia, functional abdominal pain and IBS often describe regular bowel habit but have evidence of unrecognised colonic faecal loading on AXR.…”

“…Transient lower oesophageal sphincter relaxations (TLOSRs) are the main trigger for gastro‐oesophageal reflux events. Rectal distension in dogs has been shown to increase TLOSRs to the same extent as gastric distension . Children with constipation had the same degree of oesophageal acid exposure on pH testing as those presenting with reflux symptoms .…”

“…Rectal distension in dogs has been shown to increase TLOSRs to the same extent as gastric distension. 15 Children with constipation had the same degree of oesophageal acid exposure on pH testing as those presenting with reflux symptoms. 16 In theory, stool frequency appears to be less important than the degree of colonic distension in generating functional GI and reflux symptoms.…”

Refractory Gastro-oesophageal Reflux Disease and Laryngopharyngeal Reflux - Use the Bottom up Approach

“…Hence there must be an alternative mechanism triggering TLOSRs and causing these symptoms. Studies in dogs show that rectal distension induces TLOSRs to the same extent as gastric distension [10]. Infusing fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) into the right colon increases TLOSRs and associated acid reflux events in normals.…”

“…The association between irritable bowel syndrome (IBS) and both refractory GORD and LPR suggests a common pathogenesis. IBS subjects are known to have increased sensitivity to colonic distension causing pain and increased contractility [5], but colonic distension has also been found to affect upper gut motility [6][7][8][9] and increase reflux events in physiological studies [10]. Treating GORD and LPR symptoms refractory to proton pump inhibitor (PPI) therapy remains challenging, but the effect of downstream colonic distension or occult constipation on treating GORD and LPR to date has been largely ignored.…”