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.

SUMMARY The intrinsic innervation of the human gut has been studied in strips of circular and longitudinal muscle removed at operation. Studies using drugs to stimulate the nerves within strips of human gut muscles have indicated marked regional differences in innervation (Bennett and Whitney, 1966a;Bennett, 1968;Bennett, 1970). It is of particular interest that these differences seem to correlate with regional functions and the dependence on extrinsic innervation. The drugs used were ganglion stimulants such as nicotine, which are thought to cause contraction of gut muscle by exciting cholinergic nerves and relaxation by stimulating adrenergic nerves. In brief, the experiments have indicated weak cholinergic and adrenergic intrinsic activity in human stomach (Bennett and Whitney, 1966b), suggesting a dependence of gastric motility on extrinsic (vagal) innervation. In the highly motile jejunum the intrinsic cholinergic activity overshadows the adrenergic activity (Whitney, 1965), whereas the reverse is true in the less motile colon Parks, 1963a, 1966;Bucknell and Whitney, 1964), and the terminal ileum shows an intermediate picture (Bennett, 1965). The importance of these implications makes it necessary to verify and extend the results by different methods.Since drugs might not stimulate all the nerves present, and they may produce effects unrelated to nerve activation, experiments have been made with

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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Prostaglandin‐like material was extracted from muscle and mucosa of surgically removed human stomach, ileum and colon and assayed against prostaglandin E2 on strips of rat gastric fundus. Superfused human isolated gastric mucosa released prostaglandin‐like material and release was increased by stretching or clamping the tissue. The relative amounts of extracted biological activity were broadly as follows: gastric antral mucosa > colon muscle > gastric body mucosa ≅ ileal mucosa > colon mucosa ≅ gastric muscle ≅ ileal muscle. Prostaglandin E and F were tentatively identified by chromatography and sensitivity to inactivation by alkali. Prostaglandin E apparently contributed most to the biological activity, possibly because the assay tissue is more sensitive to prostaglandin E than to F. Chromatography of gastric body mucosal extracts located material running with prostaglandin E2 and a little with E1. Colonic muscle and mucosal extracts contained material with RF values of prostaglandins E1, E2, E3 and F1α, whereas F2α and F3α‐like substances were found only in the mucosa. The proportions of prostaglandin F varied between specimens. The amount of extracted prostaglandin‐like activity was increased by adding cofactors and arachidonic acid, and lessened by homogenization with acid‐ethanol. The type and amount of activity generated from arachidonic acid by partly purified colonic mucosal prostaglandin synthetase depended on the substrate concentration. The possible relationships of prostaglandins to mucus secretion and other physiological and pathological gut functions are discussed.