Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In man, acute ethanol administration decreases lower esophageal sphincter pressure (LESP), prolongs the duration, and lowers the amplitude of esophageal contractions. These changes may contribute to gastroesophageal reflux and esophagitis. To evaluate the underlying mechanisms of these changes an animal model is needed. Hence, we studied the effect of various doses of ethanol on esophageal motility in cats, an animal with an esophagus similar to man's. Similar to man, intravenous administration of ethanol significantly decreased LESP and amplitude of lower (smooth muscle portion) esophageal contractions. It also prolonged the duration of lower esophageal contractions, even through it had no effect on contraction velocity. The effect of ethanol on upper (striated muscle portion) esophagus was different. Ethanol had no effect on the amplitude of contractions, whereas it prolonged their duration and decreased their velocity. The effect of acute ethanol on LESP in four withdrawing alcoholic cats was similar to controls. However, the acute effect of ethanol on the esophageal contractions was less marked in alcoholics. Bilateral cervical vagotomy and intravenous injection of the neurotoxin tetrodotoxin before the administration of ethanol did not prevent the effect of ethanol on LESP. This data suggests that cat esophagus is a good model for studying the underlying mechanisms of the effects of acute ethanol because its response is similar to the esophagus of man, and the acute effect of ethanol on LESP is not neurally mediated but is the result of its direct effect on muscle.
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PMID:Effect of acute ethanol on esophageal motility in cat. 202 23

The effects of ethanol upon the gastrointestinal tract (mouth, pharynx, esophagus, stomach, duodenum, Oddi's sphincter, small bowel, colon and rectum) were reviewed. Several studies showed that the incidence of cancer in the mouth and pharynx is increased in alcoholics as a consequence of ethanol effects and probably those of other compounds found in liquors. The gastroesophageal reflux disease may be induced by alcohol since it reduces the pressure in the lower and the upper esophageal sphincter, as well as the extent of primary peristalsis. Several studies showed a strong correlation between esophageal cancer and alcohol abuse. The risk for developing this kind of tumour is significantly increased when alcohol abuse and smoking coexist. Alcoholism predisposes patients to Mallory-Weiss syndrome as well as to bleeding of esophageal varices Ethanol may affect gastric secretion, motility, and permeability. Some drugs acting upon the gastric alcohol-dehydrogenase are able to affect gastric absorption of ethanol. Eradication of Helicobacter pylori increases the activity of alcohol-dehydrogenase in the pyloric antrum. The effects of alcohol upon the gastric mucosa include caustic damage, retrograde diffusion of H+, and cytoprotection. This agent may cause an acute gastritis but it is probably not involved in chronic gastritis. Whether alcohol is a risk factor for ulcer or not is unknown. Some studies found an increased incidence of gastric cancer associated with consumption of beer, wine and vodka. Some authors reported a decreased pressure in Oddi's sphincter while others found it increased in association with the consumption of ethanol. The acute and the chronic consumption of alcohol may affect the structure of small bowel as well as the absorption of nutrients. Several studies reported a significant correlation between colorectal cancer and the chronic consumption of ethanol.
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PMID:[Ethanol and the gastrointestinal tract]. 872 88

Ethanol-induced injury of digestive organs closely linked to the GI bleeding. The gastric or esophageal mucosal hemorrhage evoked by extra-amounts of alcohols is initiated by the microcirculatory damage of gastrointestinal mucosa. Many investigators focused on the ethanol-induced gastric ulcer formation as well as the ethanol-induced gastroesophageal reflux injury. Although the most important treatment for such a damage is of course to stop the drinking, it is also important to protect the gastrointestinal mucosa by potentiate the mucosal defense systems.
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PMID:[Ethanol-induced injury and GI bleeding]. 978 Jul 4