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Magnesium sulphate, a substance known to cause release of cholecystokinin (CCK) from the small intestinal mucosa, was given by mouth (dose 0·1g/kg in 150 ml water) to 20 patients with the irritable bowel syndrome. A rapid increase in colonic segmental motor activity (onset within two to six minutes in most cases) was seen (percentage activity increased from 16·2 to 23·7 <0·05; mean wave amplitude from 7·1 to 9·1 cm HO, NS; motility index from 144 to 259, <0·01). This increase was most marked in 10 patients who complained of attacks of abdominal pain after food (16·1 to 29·8%, <0·01; 6·8 to 9·6 cm HO, <0·05; 135 to 350, <0·05), and after the magnesium sulphate three of these patients experienced an attack of their usual pain. These findings provide further evidence that `functional' abdominal pain after food may in some cases be related to an exaggerated intestinal motor response to cholecystokinin. [ABSTRACT FROM PUBLISHER]

After the application of C amylopectin sulphate solution to frozen sections of human ulcer-bearing stomach, autoradiography demonstrates localization of amylopectin sulphate to the gastric surface. The affinity of amylopectin sulphate macromolecule for the gastric luminal surface would provide a substrate-bound pepsin inhibitor with a molecular sieve-like action to exclude proteolytic enzymes from the mucosal surface. This protective coating action may mimic the hypothetical role of endogenous gastric mucous substances and account for the action of amylopectin sulphate in human peptic ulcer. [ABSTRACT FROM PUBLISHER]