The lower esophageal sphincter

Abstract

Correspondence 823 Pethidine, metoclopramide and the gnstro-oesophageal sphincter Gastro-oesophageal reflux after pethidine? We were interested to read the paper by Hey ef al. (Anaesthesia 1981; 3 6. 173-6) but feel that they have failed to provide direct support for their suggestion that pethidine increases the possibility of gastro-oesopha-geal reflux, and that metoclopramide is a useful adjunct in the prevention of reflux in patients receiving pethi-dine. Their study would have been much more valuable if they had actually demonstrated acid reflux which can be easily done with an intra-oesophageal pH probe at the same time as manometric measurements. They have demonstrated lowering of lower oesophageal sphincter (LOS) pressure with pethidine and conclude that this must lead to the increased possibility of reflux because a study of Hall et a1.l quoted by them suggested that this was so. However, in contrast, atropine is also known to lower LOS pressure in man2 but it does not increase epidsodes of acid reflux.) It is true that Hall et aZ.I did find some correlation between gastro-oesophageal re-flux and lowering of the LOS pressure, this has not been the finding of other workers and there is a considerable overlap between the LOS pressure in those who reflux and the pressure in those who do not."7 Indeed Bennett6 showed that individuals with a LOS pressure as low as 8 cmH2O may not reflux whereas those with a LOS pressure as high as 32 cmHzO do. There is, therefore, a lack of precise correlation between LOS pressure and the presence or absence of reflux. This is probably related, in part, to the problem of determining a pressure reading from what is not a single pressure but a group of varying pressures which depend on the position of the manometric probe in the moreover the LOS does not have a static of fixed pressure, and it varies considerably with mechanical stress, hormonal factors, and even emotional fac-It is unwise to imply that lowering the LOS pressure with pethidine is likely to lead to reflux without demonstrating acid reflux into the oesophagus, and it is even more unwise to assume that, because metoclopra-mide appears to oppose the effect of pethidine on LOS pressure, it actually would prevent any gastro-oesopha-geal reflux that might occur. DB. The effects of premedication drugs on the lower oesophageal high pressure zone acid and reflux status of Rhesus monkeys and man. Gut 1975; 1 6 347-52. 2. LIND JS, CRISPIN JS, MCIWR DK. The effect ofatropine on the gastroesophageal sphincter. Canadian Journal of Physiology and Pharmacology 1968; 46.233-8. 3. SKINNER DB, CAMP TF. Relation of esophageal reflux to lower esophageal sphincter pressures decreased by atro-pine. Gastroenterology 1968; 54: 543-51. 4. POPE CE. A dynamic test of sphincter strength: its application to the lower esophageal sphincter. Gastroenterology 1967; 5 2 779-86. 5. HADDAD JK. Relation of gastroesophageal reflux to yield sphincter pressures. Gastroenterology 1970; 58: 175-84. 6. BENNETT JR. The physician's problem. Gut 1973; 14: 24...

Unmet Needs in the Treatment of Gastroesophageal Reflux Disease

“…The transient lower esophageal sphincter relaxation reducers, which were specifically developed to address residual acid reflux, bile reflux, or non-acid reflux, represented a promising class of drugs that failed to demonstrate efficacy in large clinical trials of patients with refractory GERD. 47 …”

The Participation of the Nitrergic Pathway in Increased Rate of Transitory Relaxation of Lower Esophageal Sphincter Induced by Rectal Distension in Dogs

“…Nitric oxide (NO) plays a major role but other inhibitory neurotransmitters may be involved such as ATP, vasoactive intestinal polypeptide (VIP), pituitary adenylate cyclaseactivating peptide (PACAP), calcitonin gene-related peptide (CGRP) and carbon monoxide (CO). Acetylcholine and Tachykinins are the main excitatory neurotransmitters; however, their contribution and the type of receptors involved in LES excitation are not completely known (3,6) . The nitrergic participation in LES motility is impractical in animal models which genetically lack neuronal NO synthase (NOS), similarly in patients with achalasia (6) .…”

“…Yet, this reflux into the esophagus is a normal phenomenon in healthy individuals, occurring primarily during episodes of transitory lower esophageal sphincter relaxation (TLESR), defined as the relaxation of the LES in absence of a swallow (17) . The TLESR is now appreciated as the most common mechanism for gastroesophageal reflux disorder (GERD), becoming a major target for new drug development initiatives (6) . Some investigations utilizing animal models characterized a neural-mediated reflex of LES relaxation during intra-gastric distention or intramural neuronal stimulation (10) .…”

Effect of Coffee on Gastroesophageal Reflux Disease

“…LES together with the crural diaphragm are the major antireflux barriers protecting the esophagus from reflux of gastric content (Hershcovici et al, 2011). Gudjonsson et al (1995) studied the effects of coffee and tea on LES function in a blinded crossover study of 12 healthy subjects.…”