. Prostaglandins E1 and E2 contracted the longitudinal muscle of human, guinea‐pig and rat isolated ileum. . The site of action varied with the species. In the rat and in some strips of human tissue prostaglandin appeared to have only a direct action on or in the muscle cells. In the other strips of human tissue and in guinea‐pig ileum the prostaglandins seemed to stimulate both the intrinsic cholinergic nerves and the muscle cells. . In contrast to the longitudinal muscle, the circular muscle of human, guinea‐pig and rat isolated ileum was usually inhibited by prostaglandin, apparently by an action directly on the muscle cells. . Prostaglandins may play a part in the control of intestinal motility.

Prostaglandins F1α and F2α caused contraction of the longitudinal muscle of both guinea‐pig isolated ileum and colon, apparently by acting directly on the muscle and on cholinergic nerves. They had little effect on ileal circular muscle. Prostaglandins E1 and E2 caused contraction of the longitudinal muscle of guinea‐pig isolated colon, apparently by acting directly on the muscle and on excitatory nerves which are non‐cholinergic. Prostaglandin E1 seems more effective than E2 in stimulating these nerves. It seems likely that prostaglandin release in vitro maintains the tone of the longitudinal muscle of guinea‐pig colon, whereas release of a prostaglandin E compound inhibits circular muscle tone.

Subjects deficient in lactase may experience bloating, cramps and diarrhoea after ingesting milk, due to the unhydrolysed and poorly-absorbed lactose. The diarrhoea may result from an osmotic effect of the lactose itself or its poorly-absorbed acidic products of fermentation (Weijers, van de Kamer & others, 1961; Christopher & Bayless, 1971), possibly together with an alteration of sodium and water absorption due to the lowered colonic pH (Rousseau & Sladen, 1971). Laxation by lactulose (1-4-beta-galactosidofructose) may operate through an analogous mechanism. The drug is a synthetic dissaccharide which, in oral doses of 10-20 g, relieves chronic constipation (Wesselius-de Casparis, Braadbaart & others, 1968). It is neither hydrolysed by intestinal dissaccharidase (Dahlqvist & Gryboski, 1965) nor absorbed in the gut, but it is converted in the colon mainly to lactic and acetic acids by various bacteria including Lactobacillus acidophilus. Apart from the increased osmotic effect, the pH in the proximal colon falls markedly (Bown, Gibson & others, 1974), and larger doses may reduce stool pH. Weijers & others (1961) inferred that the acidic products formed from lactose in the colon stimulate propulsion, and K.S. Liem (Philips-Duphar) suggested to us that lactulose may relieve constipation partly by stimulation of propulsion due to the lowered pH. The experiments described below support this view.

3 Aspirin (20-100 Rtg/ml) or indomethacin (1-4 ±g/ml) applied serosally greatly inhibited all aspects of peristalsis in guinea-pig ileum and colon. Inhibition of peristalsis of the ileum by aspirin was antagonized by prostaglandin E2 and that by indomethacin was removed by prostaglandin F2a or ACh. Inhibition of colonic peristalsis by aspirin was antagonized by prostaglandin E2 but rarely by ACh, and that by indomethacin by prostaglandin El or E2. Mucosal application of aspirin had little effect on either ileum or colon but indomethacin caused some inhibition. 4 These results support the supposition that prostaglandins contribute to peristaltic activity.

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