Effects of cholecystokinin-octapeptide and cerulein on small-intestinal motility in sheep

Cholecystokinin (CCK) affects the intestinal motility but in ruminants the question has not been entirely explored. The aim of this study was to examine the precise effects of CCK-octapeptide (CCK-OP)<br />and its amphibian analogue, cerulein, on duodenal motor activity in unfasted rams in the course of chronic experiments. Five rams underwent the implantation of a strain gauge force transducer to the duodenal wall, and &ndash; additionally &ndash; the bipolar platinum electrodes to the duodenal bulb, distal duodenum, near the strain gauge force transducer, and proximal jejunum. During continuous motor recordings, 0.15M NaCl or CCK peptides were administrated intravenously. Injections of CCK-OP at doses of 20 (over 30 s), 200 (over 30 or 60 s), and 2 000 (over 30, 60, or 120 s) ng/kg of body weight and injections of cerulein at doses of 1, 10, or 100 ng/kg (given over the same periods) were each administered in the course of duodenal phase 1, 2a, or 2b of the migrating motor complex (MMC), i.e. 5 min after the onset of each phase. Injections of the smallest doses of CCK peptides exerted a slight and mostly insignificant effect on the duodenal areas under contraction (AUC). In the duodenum, the moderate doses of the hormones evoked short stimulatory effects followed by longer inhibitory biphasic effects on AUC. These effects were inversely related to the duration of the hormone injection. It is concluded that CCK evokes stimulatory and inhibitory (biphasic) physiological effects on duodenal motility in sheep. &nbsp;

A 5-HT4 agonist mosapride enhances rectorectal and rectoanal reflexes in guinea pigs

The rectal distension-evoked reflex rectal (R-R) contractions and internal anal sphincter (R-IAS) relaxations in guinea pigs were generated through the extrinsic sacral excitatory nerve pathway (pelvic nerves) and the intrinsic cholinergic excitatory and nitrergic inhibitory nerve pathways. The aim of the present study was to evaluate whether a prokinetic benzamide, mosapride, enhances the R-R and R-IAS reflexes mediated via 5-HT4 receptors in the guinea pig. The mechanical activities of the R and IAS were recorded with a balloon connected to a pressure transducer and a strain gauge force transducer in the anesthetized guinea pig with intact spinal-intestinal pathways. Gradual and sustained rectal distension evoked R-R contractions and synchronous R-IAS relaxations. Mosapride (0.1–1.0 mg/kg iv) dose-dependently enhanced both R-R and R-IAS reflex responses. Reflex indexes for R-R and R-IAS maximally increased from 1.0 (control) to 1.92 and 1.88, respectively. A specific 5-HT4 receptor antagonist, GR 113808 (1.0 mg/kg iv), antagonized the enhancement of the R-R and R-IAS reflexes induced by mosapride 1.0 mg/kg iv. The present results indicate that mosapride enhanced the R-R and R-IAS reflexes mediated through 5-HT4 receptors.

Integrative control of rectoanal reflex in guinea pigs through lumbar colonic nerves

The aim of the present study was to analyze the neuromodulation of rectoanal reflex activity by lumbar sympathetic nerves in guinea pigs. The mechanical activities of the rectum were recorded with a balloon connected to a pressure transducer, and those of the internal anal sphincter (IAS) were recorded with a custom-made strain gauge force transducer. Gradual and sustained rectal distension evoked the rectoanal reflex, causing cholinergic contractions of the rectum and synchronous nitrergic relaxations of the IAS. Section of the lumbar colonic nerves enhanced both rectal contractions and IAS relaxations. Section of the 13th thoracic cord abolished both rectal contractions and IAS relaxations, but section of the lumbar colonic nerves restored them. Lumbar sympathectomy and pithing sacral cords greatly diminished these rectal contractions and IAS relaxations, but the intrinsic reflex component remained. N G-nitro-l-arginine methyl ester enhanced the intrinsic reflex-mediated contraction of the rectum and abolished reflex-mediated relaxation of the IAS and converted into cholinergic contractions. The present results indicate that the extrinsic lumbar inhibitory outflow causes marked inhibition of the rectoanal reflex via the lumbar colonic nerves.