Involvement of peripheral and central motor and secretory components in the action of a prostaglandin E2 analogue on colonic transit in rats

Abstract

AbstractThe effects of central and peripheral administration of a prostaglandin E2 analogue (enprostil) on colonic transit time, faecal dry matter and colonic myoelectrical activity, were examined in rats chronically fitted with a cannula in a lateral ventricle of the brain and a catheter inserted in the lumen of the proximal colon, or nichrome electrodes implanted on the proximal colon. In control studies, the mean retention time (MRT) of a marker ([51Cr] sodium chromate) administered into the proximal colon and determined in the faeces collected at hourly intervals was 7.3 ± 1.7 h, the frequency of colonic long spike bursts was 59.1 ± 9.1/h and faecal dry matter (DM) 65.4 ± 3.4%. Enprostil administered orally (350 μg/kg) decreased colonic MRT (4.9 ± 0.6 h) and faecal DM (50.1 ± 3.2%) and increased by 68% the colonic myoelectric index. Administered intracerebroventricularly enprostil (12 μg/kg) also accelerated colonic transit (MRT = 5.1 ± 1.6 h) and decreased faecal DM (48.7 ± 3.4%) but did not modify colonic spiking activity. Intraperitonal administration of the PG receptor antagonist SC‐19220 (1 mg/kg) did not affect the effects of enprostil administered centrally on MRT and DM but blocked the action of oral enprostil on colonic transit time, DM and colonic spiking activity. Centrally administered, SC‐19220 (100 μg/kg) antagonized the effects of oral enprostil on colonic transit and faecal DM but not on colonic spiking activity. It is concluded that in rats the enprostil‐induced acceleration of colonic transit involves a peripheral action on colonic motility and a secretory component which is centrally mediated. Moreover these results show that colonic hypersecretion, but not hypermotility, can alone accelerate colonic transit.