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Background: Chronic opioid use can induce esophageal dysfunction with symptoms resembling achalasia and a manometric pattern of esophagogastric junction—outflow obstruction (EGJ‐OO). However, the effect of opioids in acute setting on pharyngeal function and esophageal body contractility has not been investigated. Methods: After positioning the high‐resolution impedance manometry (HRiM) catheter, codeine (60 mg) or placebo (glucose syrup) was infused intragastrically. Forty‐five minutes post‐infusion, participants received liquid, semi‐solid, and solid boluses to assess esophageal and pharyngeal function. HRiM analysis was performed adhering to the Chicago classification v3.0. (CC v3.0). Pressure flow analysis (PFA) for the esophageal body and the pharynx was performed using the SwallowGateway™ online platform. Key Results: Nineteen healthy volunteers (HV) [5 male; age 38.3] were included. After codeine administration, higher integrated relaxation pressure 4 s values resulted in significantly reduced deglutitive EGJ relaxation and distal latency was significantly shorter. Distal contractility was similar in both conditions. Bolus flow resistance at the EGJ and distention pressures increased significantly after codeine infusion. Based on CC v3.0, acute infusion of codeine induced EGJ‐OO in six HV (p = 0.0003 vs. placebo). Codeine administration induced no significant alterations in any of the pharyngeal PFA metrics. Conclusions & Inferences: In HV, acute administration of codeine increased bolus resistance at the EGJ secondary to induced incomplete EGJ relaxation leading to major motility disorders in a subset of subjects including EGJ‐OO. However, an acute single dose of codeine did not affect motility or bolus flow in pharynx and UES. ClinicalTrials.gov number, NCT03784105. [ABSTRACT FROM AUTHOR]

The following on surgical treatments for Barrett's esophagus includes commentaries on the indications for antireflux surgery after medical treatment; the effects of the various procedures on the lower esophageal sphincter; the role of impaired esophageal motility and delayed gastric emptying in the choice of the surgical procedure; indications for associated highly selective vagotomy, duodenal switch, and gastric electrical stimulation; therapeutic strategies for detection and treatment of shortened esophagus; the role of antireflux surgery on the regression of metaplastic mucosa and the risk of malignant progression; the detection of asymptomatic reflux brfore bariatric surgery; the role of non-GERD symptoms on the results of surgery; and the indications of Collis gastroplasty and choice of the type of fundoplication. [ABSTRACT FROM AUTHOR]

The aim of this study was to explore the myenteric mechanisms of control of human esophageal motility and the effect of nitrergic and nonnitrergic neurotransmitters. Human circular esophageal strips were studied in organ baths and with microelectrodes. Responses following electrical field stimulation (EFS) of enteric motoneurons (EMNs) or through nicotinic acetylcholine receptors were compared in the esophageal body (EB) and in clasp and sling regions in the lower esophageal sphincter (LES). In clasp LES strips: 1) sodium nitroprusside (1 nM to 100 μM), adenosine-5′-[β-thio]diphosphate trilithium salt (1-100 μM), and vasoactive intestinal peptide (1 nM to 1 μM) caused a relaxation; 2) 1 mM Nω-nitro-l-arginine (l-NNA) shifted the EFS "on"-relaxation to an "off"-relaxation, partly antagonized by 10 μM 2′-deoxy-N6-methyladenosine 3′,5′-bisphosphate tetrasodium salt (MRS2179) or 10 U/ml α-chymotrypsin; and 3) nicotine-relaxation (100 μM) was mainly antagonized by l-NNA, and only partly by MRS2179 or a-chymotrypsin. In sling LES fibers, EFS and nicotine relaxation was abolished by l-NNA. In the EB, l-NNA blocked the latency period, and MRS2179 reduced "off"-contraction. The amplitude of cholinergic contraction decreased from the EB to both LES sides. EFS induced a monophasic inhibitory junction potential in clasp, sling, and EB fibers abolished by l-NNA. Our study shows a regional specialization to stimulation of EMNs in the human esophagus, with stronger inhibitory responses in clasp LES fibers and stronger cholinergic excitatory responses in the EB. Inhibitory responses are mainly triggered by nitrergic EMNs mediating the inhibitory junction potentials in the LES and EB, EFS on-relaxation in clasp and sling LES sides, and latency in the EB. We also found a minor role for purines (through P2Y1 receptors) and vasoactive intestinal peptide-mediating part of nonnitrergic clasp LES relaxation. [ABSTRACT FROM AUTHOR]