Effects of intestinal secretagogues and distension on small bowel myoelectric activity in fasted and fed conscious dogs

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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Postprandial inhibition of canine enteric interdigestive myoelectric complex

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1983.244.2.g160 ◽

1983 ◽

Vol 244 (2) ◽

pp. G160-G164

Author(s):

J. Heppell ◽

J. M. Becker ◽

K. A. Kelly ◽

A. R. Zinsmeister

Keyword(s):

Small Bowel ◽

Conscious Dogs ◽

Jejunal Loop ◽

Myoelectric Activity ◽

Proximal Jejunum ◽

Feedback Mechanisms ◽

Hormonal Factors ◽

Local Factors ◽

Recording Electrodes

Our aim was to determine whether the passage of postprandial duodenal chyme into the jejunum activates jejunal feedback mechanisms that inhibit the interdigestive myoelectric complex (IMC) of the canine small bowel. In five conscious dogs with 75-cm Vella loops of proximal jejunum and recording electrodes on the duodenum and the loop, intestinal myoelectric activity was recorded for approximately 4 h during fasting. The dogs were then given either a 200-g liver meal orally or they underwent perfusion of the jejunal loop with postprandial duodenal chyme collected from a donor dog given an identical liver meal. Before feeding, IMCs occurred at mean intervals of 126 +/- 16 (SE) min in the duodenum and 88 +/- 10 min in the loop. Feeding by mouth completely inhibited the IMCs in the duodenum but failed to inhibit the IMCs in the loop. However, perfusion of the jejunal loop with duodenal chyme suppressed the IMCs in both the loop and the duodenum. We concluded that postprandial inhibition of duodenal IMCs is mediated in part by neural and/or hormonal factors activated by chyme in the jejunum, whereas local factors inhibit jejunal IMCs. An enteric phase of postprandial IMC inhibition is postulated.

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Role of histamine H1- and H2-receptors in myoelectric activity of small bowel in the dog

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1980.238.1.g50 ◽

1980 ◽

Vol 238 (1) ◽

pp. G50-G56

Author(s):

S. J. Konturek ◽

R. Siebers

Keyword(s):

Small Bowel ◽

Receptor Antagonist ◽

Intestinal Motility ◽

Receptor Agonist ◽

Physiological Role ◽

Myoelectric Activity ◽

H1 Receptor ◽

H2 Receptor Antagonist ◽

H2 Receptor ◽

H2 Receptors

Studies were conducted in conscious dogs implanted with monopolar silver electrodes along the small intestine to determine whether the intestinal motility response to histamine is mediated by H1-receptors alone or whether H2-receptors are also involved in the response. Histamine infusion alone induced a marked increase in the appearance rate and the propagation velocity of the interdigestive myoelectric complexes (IMC). This effect was reproduced by the administration of the selective H1-receptor agonist, 2-methylhistamine, and abolished by the H1-receptor antagonist, tripelennamine. Tripelennamine alone decreased the frequency of occurrence of the IMC in fasted animals and reduced significantly the spike potential activity of the small bowel in fed dogs. Neither the H2-receptor agonist, dimaprit, nor the H2-receptor antagonist, metiamide, had any influence on the motility patterns in fasted or fed animals. We conclude that histamine influences the patterns of small bowel motility via stimulation of H1-receptors but its physiological role in modulating intestinal motility remains to be determined.

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Myoelectric Activity of the Small Bowel in Mechanical Obstruction and Intra-Abdominal Bacterial Contamination

European Surgical Research ◽

10.1159/000128778 ◽

1988 ◽

Vol 20 (5-6) ◽

pp. 304-309 ◽

Cited By ~ 1

Author(s):

M. Lausen ◽

D. Reichenbacher ◽

G. Ruf ◽

U. Schöffel ◽

K. Pelz

Keyword(s):

Small Bowel ◽

Bacterial Contamination ◽

Myoelectric Activity ◽

Mechanical Obstruction

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Effect of secretin on electrical activity of small intestine

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1975.229.2.484 ◽

1975 ◽

Vol 229 (2) ◽

pp. 484-488 ◽

Cited By ~ 27

Author(s):

AK Mukhopadhyay ◽

LR Johnson ◽

EM Copeland ◽

NW Weisbrodt

Keyword(s):

Small Intestine ◽

Small Bowel ◽

Electrical Activity ◽

Slow Wave ◽

Intravenous Infusion ◽

Action Potentials ◽

Slow Waves ◽

Wave Frequency ◽

Conscious Dogs ◽

Total Percentage

The effect of intravenously administered secretin (0.5, 2.0, 6.0 U/kg-h) and intraduodenal acidification (13.2 meq/h HCl) on the electrical activity of the small bowel of three conscious dogs with gastric and duodenal cannulas was observed. Electrical activity was recorded in fasted as well as fed conditions through silver wire electrodes implanted along the entire length of the small bowel. Intravenous infusion of secretin in all dosages and in all dogs delayed the onset of the interdigestive myoelectric complex and reduced the total percentage of slow waves with superimposed spike potentials. Intraduodenal acidification also inhibited the interdigestive myoelectric complex, which developed incompletely with fewer action potentials on slow waves. Secretin did not produce any alteration in the fed pattern of activity, slow-wave frequency, or the caudal migration of the interdigestive myoelectric complex. The present study indicates that the nuerohumoral mechanisms responsible for initiation of the interdigestive myoelectric complex may be different from those responsible for its caudal migration.

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Somatostatin induces ectopic activity fronts via a local intestinal mechanism during fed state or pentagastrin

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1986.250.2.g149 ◽

1986 ◽

Vol 250 (2) ◽

pp. G149-G154

Author(s):

E. Schippers ◽

J. Janssens ◽

G. Vantrappen ◽

M. Vandeweerd ◽

T. L. Peeters

Keyword(s):

Small Bowel ◽

Myoelectric Activity ◽

Dependent Manner ◽

Ectopic Activity ◽

Fed State ◽

Small Bowel Motility ◽

Bipolar Electrodes ◽

Jejunal Segment ◽

Small Branch ◽

Local Release

The effect of local intra-arterial infusions of somatostatin on small bowel motility in the postprandial period and during an intravenous pentagastrin infusion was studied in five dogs. A Silastic catheter was implanted in a small branch of the superior mesenteric artery perfusing a 5-to 10-cm jejunal segment located 30-40 cm distally to Treitz. Small bowel myoelectric activity was recorded by means of a series of bipolar electrodes implanted subserosally along the small intestine. Experiments were started 2 wk after surgery and were performed in conscious animals. Intra-arterial infusion of somatostatin induced activity fronts in the fed state and during intravenous pentagastrin infusion in a dose-dependent manner. These activity fronts always started at or just below the perfused segment, migrated distally over the remaining small bowel, and were superimposed on the fed pattern. We conclude that local administration of somatostatin is able to initiate normally migrating ectopic activity fronts, despite the presence of neural and hormonal factors that control the fed state. Local release of somatostatin might be involved in the initiation of spontaneously occurring activity fronts.

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Effect of cholecystokinin on myoelectric activity of small bowel of the dog.

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1977.232.1.e44 ◽

1977 ◽

Vol 232 (1) ◽

pp. E44

Author(s):

A K Mukhopadhyay ◽

P J Thor ◽

E M Copeland ◽

L R Johnson ◽

N W Weisbrodt

Keyword(s):

Small Intestine ◽

Small Bowel ◽

Protein Secretion ◽

Myoelectric Activity ◽

Fed State ◽

Small Bowel Motility ◽

Intraduodenal Infusion ◽

Dose Dependent Increase ◽

Dose Dependent ◽

Made In

The effect of cholecystokinin on the myoelectric activity of the small intestine was determined in conscious dogs. Six animals were implanted with electrodes along the small intestine, and a cannula was placed in the stomach. A second cannula was inserted into the duodenum in three animals, and a pancreatic fistula was prepared in three animals. Recordings were made in the fasted state, during the intravenous infusion of either saline or cholecystokinin-octapeptide (CCK-OP), during the intraduodenal infusion of either saline or L-tryptophan, and during the fed state. CCK-OP disrupted the fasted pattern of myoelectric activity, caused a dose-dependent increase in spike potentials, and caused a dose-dependent increases in pancreatic protein secretion. Stimulation of myoelectric activity occurred at doses that produced submaximal protein secretion; however, the stimulation was not identical to that seen with feeding. Intraduodenal infusion of L-tryptophan increased pancreatic protein secretion, interrupted the fasted pattern of motility, and induced a pattern similar to that seen with feeding. We conclude that CCK alters small intestinal motility and may play a role in the changes in small-bowel motility caused by the ingestion of food.

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Inhibition of canine interdigestive proximal gastric motility by cholecystokinin octapeptide

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1981.240.3.g217 ◽

1981 ◽

Vol 240 (3) ◽

pp. G217-G220

Author(s):

J. C. Schang ◽

K. A. Kelly

Keyword(s):

Gastric Motility ◽

Conscious Dogs ◽

Intraluminal Pressure ◽

Myoelectric Activity ◽

Cyclic Activity ◽

Proximal Stomach ◽

Cholecystokinin Octapeptide ◽

Interdigestive Motility

Feeding abolishes cyclic interdigestive motility and decreases intraluminal pressure in autotransplanted pouches of canine proximal stomach. Our aim was to determine whether cholecystokinin might be the hormonal messenger involved. In four conscious dogs with autotransplanted proximal gastric pouches and chronic duodenal electrodes, intrapouch pressure and duodenal myoelectric activity were measured during fasting, while cholecystokinin octapeptide (CCK-OP) was infused intravenously for 4 h at doses 0, 15, 31, 62, 125, and 250 mg . kg-1 . h-1. Each dose was given five times to each animal. Cholecystokinin octapeptide inhibited the interdigestive cycles in both pouch and duodenum and decreased the pressure in the pouch. The threshold for these effects was 31 ng . kg-1 . h-1, and the ED50 was 62 ng . kg-1 . h-1. The dose of 125 ng . kg-1 . h-1 suppressed the cycles nearly completely and decreased mean +/- SE intrapouch pressure from 15.3 +/- 1.1 to 6.3 +/- 2.8 cmH2O . min (P less than 0.001). After the infusions were stopped, cyclic activity and intrapouch pressure returned promptly to control values. We concluded that CCK-OP at "physiological" doses abolished interdigestive cycles and decreased intraluminal pressure in autotransplanted pouches of canine proximal stomach.

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