Effect of ethanol upon gastric emptying.

Abstract

SUMMARY The effect of ethanol upon gastric emptying in healthy human subjects was studied by measuring the gastric emptying rates of three 750 ml meals, the osmolalities, energy densities, and pH of which were similar. Meal A, which contained 80 ml alcohol, emptied more rapidly than meal B, which contained 40 ml ethanol and 63-3 g dextrose; and meal B emptied more rapidly than meal C, which contained 126-6 g dextrose but no ethanol. The slower rate of emptying of the dextrose meal (C) was not due to an increased gastric secretory rate, as serial measurements of gastric pH were substantially and significantly higher with this than with the other two meals; nor was it due to a greater degree of duodenogastric reflux, as serial measurements of gastric bile acid concentrations were similar for the three meals. We conclude that the duodenal osmoreceptor mechanism is relatively insensitive to ethanol; that the relationship between energy density and gastric emptying rate does not hold in the case of ethanol; and that the gastro-oesophageal reflux which occurs in response to ethanol is not due to impairment of gastric emptying.Recently we reported that alcohol induces gastrooesophageal reflux in healthy individuals (Kaufman and Kaye, 1978

Alcohol-Related Diseases of the Esophagus and Stomach

“…This inhibitory effect by ethanol solutions is not dosedependent [47,48] and is not induced by their caloric content, since isocaloric glucose solutions have a more pronounced inhibitory effect [48,49] .…”

Effect of ethanol and some alcoholic beverages on gastric emptying in humans

“…The few published studies on the effects of alcoholic beverages or ethanol on gastric emptying showed that ethanol in concentrations of 8%, 12% and 16% (w/v) delayed gastric emptying compared with both water and a lower ethanol concentration (6% w/v) (1,2). Gastric emptying was inhibited by glucose to a larger degree than by isocaloric amounts of ethanol (3). Red wine was emptied at almost the same rate as dealcoholized, isocaloric red wine (4).…”

Alcohol and Smoking

“…Franke et al [34] recently confirmed the inhibitory effect of ethanol and detected inhibition even at low ethanol concentrations (4% v/v). This inhibitory effect by ethanol solutions is not dose-dependent [33,34] and is not induced by their caloric content, since isocaloric glucose solutions have a more pronounced inhibitory effect [17,34]. …”

“…It was demonstrated in cats that ethanol also has direct effects on the smooth musculature of the lower esophageal sphincter [15]. A decrease in lower esophageal sphincter pressure and inhibition of the primary peristalsis of the distal esophagus induced by ethanol result in an increase in the frequency of gastroesophageal reflux (by up to 90%) and in a prolongation of each reflux episode by diminishing esophageal clearance [16,17]. These effects are dose-dependent and start with a threshold dose of 45–60 g ethanol or at blood ethanol concentrations of 70–90 mg/dl [18].…”

“…Additionally, one multicenter case-control study has shown that alcohol consumption may be a possible risk factor for the development of esophagitis and/or Barrett’s esophagus [25]. Besides the induction of esophagitis due to an increased gastroesophageal acid reflux, alcohol itself might impair the esophageal mucosa [13,14,15,16,17,18,19,20,21,22]. For example, Chung et al [26] have shown in rabbits that ethanol perfusion (5% v/v adjusted with sodium chloride to a total ionic concentration of 300 m M ) markedly increased the rate of removal of H + from the esophageal lumen with an accompanying fall in the transmural potential difference.…”