The role of accelerated colonic transit in prostaglandin‐induced diarrhoea and its inhibition by prostacyclin

• Published in: British journal of pharmacology 1984-09, Vol.83 (1), p.157-159
• Main Authors: Rush, Bob D., Ruwart, Mary J.
• Format: Article
• Language: English
• Subjects: 16,16-Dimethylprostaglandin E2 - pharmacology; Animals; Colon - drug effects; Diarrhea - chemically induced; Diarrhea - physiopathology; Diarrhea - prevention & control; Epoprostenol - pharmacology; Gastrointestinal Motility - drug effects; Male; Prostaglandins - pharmacology; Rats
• ISSN: 0007-1188; 1476-5381
• DOI: 10.1111/j.1476-5381.1984.tb10130.x

1 Rats treated with subcutaneous 16,16‐dimethyl prostaglandin E2 (16,16‐dimethyl PGE2, 100 μg kg−1) exhibited diarrhoea even when their ileo‐caecal junctions were tied, thereby eliminating contributions from small intestinal transit or fluid accumulation (enteropooling). 2 The origin of the watery stool appeared to be the caecum, since tying the caecal‐colonic junction eliminated it. 3 The acceleration of colonic transit is likely to be a primary mechanism of PGE2‐induced diarrhoea in the rat, since both normal animals and those with tied ileo‐caecal junctions exhibited almost the same incidence of diarrhoea. 4 Subcutaneous prostacyclin (PGI2) (2 mg kg−1 every 60 min) suppressed 16, 16‐dimethyl PGE2‐induced diarrhoea in normal rats and in those with tied ileo‐caecal junctions. 5 Colonic transit measured in rats with cannula preimplanted in their proximal colon indicated that 16, 16‐dimethyl PGE2 enhanced colonic transit and PGI2 suppressed this increase. Thus, PGI2 can inhibit diarrhoea in the rat caused by 16, 16‐dimethyl PGE2 by suppressing colonic transit exclusive of its effects on small intestinal transit and enteropooling.