[Mutual relationship between the gastroscopic picture, HCl secretion and histological findings on the stomach mucosa following resection of the stomach].
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This study was designed to assess the gastric secretory effects of ebrotidine, a novel H2 receptor antagonist, in humans. Three groups (A, B and C) of male subjects with normal gastric mucosa were used. Group A (6 subjects) was used to determine the dose-dependency of gastric inhibitory effect of ebrotidine on basal and pentagastrin-induced maximal acid output. Group B (8 subjects) was employed to examine the duration of the inhibitory effect of ebrotidine on basal and pentagastrin-induced acid secretion. In group C (6 subjects), the 24h pH-metry was assessed using intraluminal pH-electrode placed in the gastric corpus and connected to a portable recording unit. Single oral dose of ebrotidine (200, 400 or 800 mg) caused a dose-dependent reduction in basal and pentagastrin-induced acid secretion that at a dose of 800 mg amounted to about 89% and 93%, respectively. This inhibition was still observed after 6h and averaged 72% and 50%, respectively. After 12 and 24h upon the drug intake, both basal and pentagastrin-induced acid secretion returned to the control values. Single oral dose of ebrotidine (800 mg) caused a significant reduction in circadian acidity and resulted in a marked and significant reduction of intragastric acidity for about 6h upon the administration. This inhibition was accompanied by a transient increase in basal and postprandial gastrin levels. We conclude that ebrotidine is highly effective inhibitor of basal, pentagastrin-induced and circadian gastric acid secretion in humans.
The authors studied acid and nonparietal secretion and the level of the blood flow in the gastric mucosa combined with the determination in it of the concentrations of prostaglandins (PGE and PGF2 alpha) and cyclic nucleotides (cAMP and cGMP) in 39 patients with primary (mostly medio-gastric) gastric ulcers, in 22 patients with secondary gastric lesions (with relation to duodenal ulcer) and in 58 patients with peptic ulcer. 30 healthy persons were investigated for control. More active acid secretion of the stomach was shown in the patients with secondary ulcers (as compared to the patients with primary ulcers) with similar indices of bicarbonate and fucose. The deficit of PGE in gastric mucosa was observed in ulcers of different sites with its lowest values in secondary gastric ulcers. In the patients with primary and secondary gastric ulcers the level of mucosal PGF2 alpha was decreased, in duodenal ulcer it was normal. A higher rate of the gastric blood flow was observed in the patients with duodenal and secondary gastric ulcers, and a normal one-in primary gastric ulcers. Normal gastrinemia was noted in ulcers of different sites. The development of secondary gastric ulcers in patients with duodenal ulcers appeared to result from insufficiency of prostaglandin biosynthesis in the gastric mucosa.
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In animal and human studies, the gastric emptying of large (greater than 1 mm) indigestible solids is due to the activity of the interdigestive migrating myoelectric complex. The gastric residence time (GRT) of an orally administered, nondigestible, pH-sensitive, radiotelemetric device (Heidelberg capsule) was evaluated in three studies in healthy volunteers. In 6 subjects, the GRT of the Heidelberg capsule was compared with the half-emptying time (t1/2) of diethylenetriaminepentaacetic acid labeled with technetium 99m after a 4-ml/kg liquid fatty meal. The mean (+/-SD) GRT (4.3 +/- 1.4 h) was significantly (p less than 0.001) longer than the mean t1/2 (1.1 +/- 0.3 h); the GRT was prolonged compared with the t1/2 in each subject. In a randomized, crossover trial in 10 subjects, frequent feeding caused a dramatic prolongation in mean GRT of the capsule compared with the fasting state (greater than 14.5 vs. 0.5 h, p less than 0.005). In another crossover study in 6 subjects, the GRT of the capsule was evaluated after an overnight fast, a standard breakfast including solid food, and a liquid meal (i.e., 200 ml of diluted light cream). The mean GRT was 2.6 +/- 0.9 h after the liquid meal vs. 1.2 +/- 0.8 h after fasting (p less than 0.025). The mean GRT after the breakfast was 4.8 +/- 1.5 h, which was significantly greater than that after fasting (p less than 0.001) and after the liquid meal (p less than 0.01). These data suggest that the GRT of the Heidelberg capsule is a marker of the interdigestive migrating myoelectric complex in humans, the interdigestive migrating myoelectric complex can be markedly delayed by frequent feedings with solids, and the interdigestive migrating myoelectric complex is delayed by both liquid and solid meals.
To study the effects on gastric content and subjective well being of chewing gum in the immediate preoperative period, 60 female nonsmokers were randomized to use regular, sugar-free chewing gum preoperatively or to continue the overnight fast. In a similar fashion 44 habitual smokers were randomized to use nicotine gum 2 mg or not. Nonsmokers using chewing gum had significantly larger gastric fluid volumes than controls (mean 30 +/- 19 mL vs 20 +/- 15 mL; 95% confidence interval (CI) for difference 1-19 mL; P = 0.03), with no difference in gastric fluid acidity. In smokers, neither gastric fluid volume nor acidity differed significantly between those who were or were not chewing gum. Although the use of nicotine gum in smokers was associated with a reduction in dryness of the mouth, thirst, and irritability, nonsmokers chewing regular gum did not report significant improvements in patient well being. In habitual smokers unable to abstain from nicotine, the use of nicotine gum on the morning of surgery may be beneficial. Although it is difficult to prove a direct influence on the incidence of pulmonary aspiration of increased gastric contents, the fact that regular, sugar-free chewing gum increased gastric fluid volumes probably means that it should not be used on the morning of surgery.
BACKGROUND AND AIM: Duodenal acidification might increase sensitivity to gastric distension, which seems to play a role in the genesis of dyspeptic symptoms in a subset of patients with functional dyspepsia. The aim of the present study was to investigate the characteristics of dyspeptic symptoms associated with hypersensitivity to gastric distension induced by duodenal acidification. METHODS: An infusion tube and a barostat bag were positioned in the duodenum and gastric fundus, respectively. Sensitivity to stepwise fundic distensions with severity scoring of the seven dyspeptic symptoms was assessed before and during duodenal acid infusion in 20 healthy subjects. RESULTS: Acid infusion significantly decreased the pressures and the corresponding wall tensions at the thresholds for discomfort. At the distending level of minimal distending pressure (MDP) + 2 mmHg, significantly higher scores of fullness and bloating were obtained during acid infusion. With distending stimuli of MDP + 4 and 6 mmHg, fullness, bloating, nausea, satiety, epigastric burning and epigastric pain were significantly more severe during acid infusion than before acid infusion. At the level of MDP + 8 mmHg, the severity of epigastric pain was significantly greater, compared with that before acid infusion. CONCLUSIONS: Duodenal acidification might aggravate dyspeptic symptoms through the induction of hypersensitivity to gastric distension in healthy individuals. Those symptoms are diverse and variable, depending on the strength of the distending stimuli.
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The effect of carbenoxolone on taurocholate-induced changes in gastric mucosal permeabiity was assessed in three dogs, each of which was prepared with an antrectomy and a vagally denervated gastric pouch. Perfusion of the canine pouches with sodium taurocholate (40 mM) was associated with an increase in hydrogen ion back diffusion. This effect was not diminished by 10 days of carbenoxolone treatment. The effect of carbenoxolone on ethanol-induced changes in gastric mucosal permeability was assessed in six normal human subjects. A significant increase of gastric mucosal permeability was observed in six normal human subjects after instillation of ethanol (20 percent v/v). After 3 weeks of oral ingestion of carbenoxolone, there was inconsistent protection against ethanol-induced increases in gastric mucosal permeability. Basal secretion of hydrogen ion and postethanol hydrogen ion secretion appear to be diminished by carbenoxolone. These studies suggest that carbenoxolone does not protect against taurocholate- and ethanol-induced increases in gastric mucosal permeability in the dog and in man. It seems unlikely that carbenoxolone exerts its beneficial effect on the healing of gastric ulcers in man by an effect on gastric mucosal permeability.
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