ENDOGENOUS and exogenous prostaglandins (PGs) have been implicated in the pathogenesis of diarrhoea. PGF2α may be secreted by some thyroid tumours which are accompanied by diarrhoea1; when given for the termination of pregnancy this PG produces diarrhoea as an undesirable effect2. Oral or intraluminal PGE1 speeds up intestinal transit3 and causes secretion of fluid and electrolytes into the intestine4. In animals, PGE1 and PGF2α inhibit intestinal sodium transport5 and produce loss of fluid from intestinal loops6. Isolated human intestinal muscle responds to PGs with contractions or relaxations, depending on the site and the PG used7–10. In spite of these marked effects on both the secretory and motor functions of the gut, the action of intravenous prostaglandins on human small intestinal function has not been studied. We have measured the effect of intravenous infusions of PGF2α; on the net movement of water, electrolytes, transit rate and on pressure activity in the human jejunum and ileum.