Gastric acid secretion varies cyclically with interdigestive antroduodenal motility. Acute acid inhibition with intravenous famotidine does not significantly affect interdigestive antroduodenal motility.

Maalox provides faster relief of heartburn than ranitidine. Heartburn can be assessed frequently and reliably under ambulant conditions using an electronic patient diary.

Background: Alterations in gastrointestinal motility and hormone secretion, especially activation of the ileal brake, have been documented in malabsorption. Aim: To investigate whether artificially‐induced accelerated small intestinal transit activates the ileal brake mechanism. Methods: Eight healthy volunteers (four female, four male; age 21 ± 3 years) participated in four experiments: (a) meal with either oral magnesium sulphate (MgSO4) or placebo; and (b) fasting with either oral MgSO4 or placebo. Antroduodenal motility was recorded by perfusion manometry. Duodenocaecal transit time was determined by the lactulose H2 breath test. Gall‐bladder volume was measured by ultrasound at regular intervals, and blood samples were drawn for determination of cholecystokinin and peptide YY (RIA). Twenty‐four hour faecal weight and fat excretion were determined. Results: MgS04 significantly accelerated duodenocaecal transit time and increased faecal fat and weight in all subjects. MgSO4 significantly delayed the reoccurrence of phase III and affected antroduodenal motility during fasting but not after meal ingestion. Postprandial gall‐bladder relaxation and postprandial peptide YY release were significantly increased during the MgSO4 experiment compared to placebo. Conclusions: The osmotic laxative MgS04 accelerates intestinal transit both in the fasting and fed state. MgS04 activates the ileal brake mechanism only in the fed state, with peptide YY release and inhibition of gall‐bladder emptying.

INTRODUCTIONSomatostatin and its analogue octreotide in¯uence gastrointestinal motility and secretion. 1±3 Both inhibit gastric acid and pancreatic enzyme secretion, gallbladder contraction and delay intestinal transit. Recent studies indicate that octreotide affects visceral perception by increasing the threshold for symptoms during balloon distension. This has been demonstrated for rectal and colonic perception both in healthy subjects and patients with irritable bowel syndrome.3±6 Octreotide in¯uences perception through inhibition of the spinal afferent pathway. 4,6 Little is known about the effect of somatostatin on proximal gastric motor function and symptom perception. Only Mertz et al., 7 using the long-acting somatostatin analogue octreotide, found the gastric accommodation re¯ex to be reduced, resulting in a less compliant proximal stomach. Octreotide also had an inhibitory effect on the perception of fullness in response to low volume distensions. The aim of our study was to investigate the effect of native somatostatin during continuous intravenous infusion on the motor function of the proximal stomach and visceral perception during volume and pressure distensions. The function of the proximal stomach was measured with an electronic barostat. MATERIALS AND METHODS SubjectsSix healthy volunteers (four female, two male, mean age 23 years; range 19±27 years) participated in the study. None had a history of gastrointestinal symptoms, had previously undergone abdominal surgery or was using SUMMARY Background: Somatostatin affects gastrointestinal motility and secretion and visceral sensation, but little is known about its effects on the proximal stomach. Aim: To evaluate the effects of somatostatin on proximal gastric motor function and perception of symptoms. Methods: Six healthy subjects participated in two experiments performed in random order during continuous intravenous infusion of saline or somatostatin (250 lg/h). Proximal gastric motor function was evaluated using a barostat. We performed pressure and volume distensions and a barostat procedure (minimal

(a) Basal and gastrin-17-stimulated gastric acid secretion are reduced during hyperglycaemia; (b) infusion of gastrin-17 to physiological post-prandial levels does not affect plasma PP levels; (c) plasma PP levels are reduced during hyperglycaemia, suggesting vagal-cholinergic inhibition of gastric acid secretion during hyperglycaemia.