Inhibition of Peristalsis in Guinea‐pig Isolated Ileum and Colon by Drugs That Block Prostaglandin Synthesis

Abstract

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.

Dai-kenchu-to Enhances Accelerated Small Intestinal Movement.

“…In addition, it has been suggested that there is an inhibitory effect of [6]-gingerol or [6]-shogaol on COX in vivo and in vitro, 25,26) and that PGs contribute to peristaltic activity via a direct action on the muscle cells and stimulating nerves. 27) Since it was confirmed that PGs were involved in the present models, the inhibition of COX may contribute to the inhibitory effects of dried ginger root on accelerated small intestinal motility.…”

The Contribution of Prostaglandins in the Muscle of Human Isolated Small Intestine to Neurogenic Responses

“…However, the circular and longitudinal muscle layers interact, and it is not possible to extrapolate from muscle strips to intestinal behaviour. Despite inhibition of circular muscle strips of guinea-pig colon by prostaglandin El or E2, peristaltic activity in colonic segments was increased by these compounds (Eley, Bennett & Stockley, 1977), and decreased by aspirin (Bennett, Eley & Stockley, 1976).…”

Quantitative analysis of peristalsis in the guinea‐pig small intestine using spatio‐temporal maps

“…It is likely that the circular muscle is relatively less excitable (or more inhibited) and requires considerable excitatory motor input to reach the threshold for contraction, whereas the longitudinal muscle layer is normally very close to threshold, judged by the presence of spontaneous contractions. This difference in state could be due to a preferential inhibition of circular muscle, but not longitudinal muscle, by prostaglandins released from damaged tissue (Bennett et al 1976;Maggi et al 1994). Another possibility is that the circular muscle, but not the longitudinal muscle, is actively inhibited by enteric inhibitory motor neurones.…”