Does Intravenous Ondansetron Affect the Intestinal Motility Pattern in Healthy Donkeys (Equus asinus)?

The effects of substance P (SP) on intestinal myoelectric activity were examined in conscious dogs with implanted silver electrodes on the small doses (0.25-1.0 nmol . kg-1 . h-1) raised the frequency of interdigestive myoelectric complexes and also increased preburst activity, mostly in the upper small bowel. The ileum was relatively less sensitive to the stimulatory action of sp. At higher doses (2.04.0 nmol . kg-1 . h-1) SP caused a fedlike motility pattern. In the doses used SP did not change the foodinduced motility pattern. The effects of SP on myoelectric activity were blocked by atropine or pirenzepine. We conclude that SP was participate in neurally mediated changes in intestinal motility.

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The effect of feeding on the motility of the stomach and small intestine in the pig

British Journal Of Nutrition ◽

10.1079/bjn19760045 ◽

1976 ◽

Vol 35 (3) ◽

pp. 397-405 ◽

Cited By ~ 83

Author(s):

Y. Ruckebusch ◽

L. Bueno

Keyword(s):

Small Intestine ◽

Intestinal Motility ◽

Proximal Part ◽

Standard Diet ◽

Basic Pattern ◽

Motility Pattern ◽

Continuous Activity ◽

Effect Of Feeding ◽

Spike Bursts ◽

Food Consumed

1. Electromyographical studies were made on the motility of the stomach and small intestine of five pigs when given a standard diet eitherad lib., or as one or two meals/d. Recordings were made from electrodes placed chronically on the antrum, the duodenum and the jejuno-ileum, and a continuous 24 h recording was made every 2 d for a period of 4 weeks. A simple ‘T’-shaped cannula was positioned in the proximal duodenum in two of the pigs.2. The basic pattern of activity of the small intestine was grouped in phases of irregular and regular activity characteristic of the myoelectric complex. This pattern recurred about eighteen times/d in fasting pigs, or in animals fedad lib.and so eating frequent but small meals. When a myoelectric complex on the duodenum reached its regular ‘spiking’ phase, antral activity and passage of digesta ceased completely for a period (5–15 min) which varied according to the time elasped since the last meal.3. In animals receiving one meal/d a postprandial pattern of activity lasted about 6 h. The proximal part of the intestine showed continuous activity with vigorous isolated or peristaltic spike bursts. The average number of myoelectric complexes was thirteen/d. When receiving two meals/d the postprandial pattern lasted for only 2–3 h, and approximately sixteen myoelectric complexes/d were recorded.4. It is concluded that the extent of disruption of the basic intestinal motility pattern depends on the amount of food consumed per meal and subsequent release of nutrients.

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Cholecystokinin in the regulation of intestinal motility and pancreatic secretion in dogs

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1988.255.4.g498 ◽

1988 ◽

Vol 255 (4) ◽

pp. G498-G504 ◽

Cited By ~ 4

Author(s):

P. Thor ◽

J. Laskiewicz ◽

P. Konturek ◽

S. J. Konturek

Keyword(s):

Small Bowel ◽

Spike Activity ◽

Pancreatic Secretion ◽

Intestinal Motility ◽

Motility Pattern ◽

Motor Complex ◽

Pancreatic Fistulas ◽

Cck Antagonists ◽

Cck Receptor Antagonists ◽

Stimulation Of

Peptidal (CR-1409) and nonpeptidal (L-364,718) cholecystokinin (CCK) receptor antagonists were used to determine the possible involvement of CCK in the fasted and fed intestinal motility patterns and the related alterations in pancreatic secretion. Dogs were implanted with electrodes along the small bowel and with chronic pancreatic fistulas. In fasted dogs, the typical migrating motor complex (MMC) cycles and accompanying fluctuations in pancreatic secretion were recorded. Neither of the CCK antagonists affected these motor and secretory components of the MMC. Feeding interrupted the MMC and increased spike activity at all levels of the small bowel, and this was accompanied by a significant increase in pancreatic secretion and in plasma hormone [gastrin, CCK, and pancreatic polypeptide (PP)] levels. Both CCK antagonists significantly reduced the postprandial spike activity but failed to restore the fasted pattern. Exogenous gastrin and CCK, as well as bombesin, induced fedlike motility patterns accompanied by marked pancreatic protein secretion. These effects were completely reversed to the fasted patterns during intravenous infusion of CCK antagonists. In contrast, cholinergic stimulation (bethanechol) induced a fedlike pattern that was more resistant to CCK antagonists. We conclude that CCK does not play a major role in the fasted motility pattern and related fluctuations in pancreatic secretion but may be partly involved (by itself and by released PP) in the induction of the fed motility pattern and the postprandial stimulation of the exocrine pancreas.

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Role of GIP and insulin in glucose-induced changes in intestinal motility patterns

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1987.252.1.g8 ◽

1987 ◽

Vol 252 (1) ◽

pp. G8-G12 ◽

Cited By ~ 2

Author(s):

P. Thor ◽

J. Laskiewicz ◽

J. W. Konturek ◽

S. J. Konturek ◽

W. Creutzfeldt

Keyword(s):

Spike Activity ◽

Intestinal Motility ◽

Moderate Increase ◽

Inhibitory Peptide ◽

Marked Rise ◽

Motility Pattern ◽

Insulin Levels ◽

Induced Changes ◽

Higher Doses

This study was designed to correlate the intestinal motility patterns with duodenal glucose loads and the increments in plasma gastric inhibitory peptide (GIP) and insulin levels after these loads or after the administration of exogenous hormones in conscious dogs. Isotonic glucose instilled intraduodenally at lower loads (5.2-42.4 mmol/h) only caused a moderate increase in spike activity, but at higher loads (84.8 mmol/h) it disrupted migrating myoelectric complexes (MMC), being accompanied by marked increases in plasma GIP and insulin levels. Duodenal loads of isotonic mannitol resulted in similar motility changes but without alteration in plasma GIP or insulin. Hypertonic glucose (20%) in the duodenum also caused an increase in spike activity, and at higher loads (72 mmol/h or higher) it disrupted MMCs and resulted in significant increments in plasma GIP and insulin levels. Physiological doses of exogenous GIP (25-400 pmol X kg-1 X h-1) or insulin (12-24 mU X kg-1 X h-1) did not affect the motility pattern, but at higher doses, raising plasma hormone over the levels occurring after a mixed meal, GIP (400 pmol X kg-1 X h-1) increased significantly the MMC interval, whereas insulin (48-96 pmol X kg-1 X h-1) induced a fed-like motility pattern. Intravenous 20% glucose (72 mmol/h) caused a marked rise in plasma insulin (but not GIP) levels but failed to affect the intestinal motility as did 20% mannitol infused intravenously in the same dose.(ABSTRACT TRUNCATED AT 250 WORDS)

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