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

1988 ◽  
Vol 255 (4) ◽  
pp. G498-G504 ◽  
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.

Influence of substance P on myoelectric activity of the small bowel

1982 ◽  
Vol 243 (6) ◽  
pp. G493-G496 ◽  
Author(s):  
P. J. Thor ◽  
R. Sendur ◽  
S. J. Konturek
Keyword(s):  
Small Bowel ◽  
Substance P ◽  
Intestinal Motility ◽  
Conscious Dogs ◽  
Myoelectric Activity ◽  
Stimulatory Action ◽  
Motility Pattern ◽  
Small Doses ◽  
Silver Electrodes ◽  
Higher Doses

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.

Studies on the inhibition of pancreatic secretion by luminal somatostatin

1981 ◽  
Vol 241 (2) ◽  
pp. G109-G115 ◽  
Author(s):  
S. J. Konturek ◽  
J. Tasler ◽  
M. Cieszkowski ◽  
J. Jaworek ◽  
A. Arimura ◽  
...  
Keyword(s):  
Pancreatic Secretion ◽  
Exocrine Pancreas ◽  
Inhibitory Action ◽  
Serum Gastrin ◽  
Gastrointestinal Hormones ◽  
Duodenal Mucosa ◽  
Enzyme Protein ◽  
Duodenal Acidification ◽  
Pancreatic Fistulas ◽  
Stimulation Of

The effects of somatostatin, instilled into the duodenum or administered intravenously, on pancreatic response to endogenous (meal and duodenal acidification) or exogenous (secretin and caerulein) stimulants were compared in five dogs with gastric and pancreatic fistulas. Somatostatin, whether applied topically to the duodenal mucosa or given intravenously, resulted in qualitatively similar inhibition of pancreatic secretion of water, bicarbonate, and enzyme protein, being about four to eight times less potent after intraduodenal than after intravenous administration. A meal-induced secretion appears to be the most sensitive to the inhibitory action of intraduodenal somatostatin, probably because of the suppression of gastric acid and serum gastrin secretin involved in the postprandial stimulation of the exocrine pancreas. The inhibition of pancreatic secretion by luminal somatostatin was accompanied by a significant increase of plasma levels of the immunoreactive somatostatin, indicating that this peptide can be absorbed intact across the intestinal mucosa. We conclude that somatostatin administered into the gut lumen is absorbed into the circulation and can inhibit pancreatic secretion both by the suppression of the release of gastrointestinal hormones and by direct inhibitory action on the exocrine pancreas.

Comparison of effects of neurotensin and fat on pancreatic stimulation in dogs

1983 ◽  
Vol 244 (6) ◽  
pp. G590-G598 ◽  
Author(s):  
S. J. Konturek ◽  
J. Jaworek ◽  
M. Cieszkowski ◽  
W. Pawlik ◽  
J. Kania ◽  
...  
Keyword(s):  
Protein Secretion ◽  
Pancreatic Secretion ◽  
General Circulation ◽  
Constant Ph ◽  
Equal Rate ◽  
Duodenal Acidification ◽  
Pancreatic Fistulas ◽  
Protein Response ◽  
Dose Dependent ◽  
Stimulation Of

In six conscious dogs with esophageal, gastric, and pancreatic fistulas, the effects of intravenous infusion of neurotensin and intraduodenal instillation of sodium oleate on gastric and pancreatic secretion were determined under basal conditions and after exogenous (secretin and cholecystokinin octapeptides) or endogenous stimulants (feeding and duodenal acidification). Neurotensin given intravenously in graded doses (1.5–200 pmol . kg-1 . min-1) to fasted dogs produced a dose-dependent stimulation of pancreatic bicarbonate and protein secretion reaching, respectively, about 18 and 100% of maximal responses to secretin and cholecystokinin octapeptide (CCK). Duodenal oleate in graded doses (0.5–16 mmol/h) resulted in a similar pattern of bicarbonate and protein secretion but increased plasma neurotensin only to about 10% of that achieved with infusion of exogenous neurotensin producing an equal rate of pancreatic secretion. Neurotensin, like oleate, potentiated the action of secretin and CCK on pancreatic bicarbonate and had additive effects on protein response to these secretagogues. Both neurotensin and oleate increased pancreatic response to liver extract meal kept in the stomach at constant pH (5.5) and the response to sham feeding but decreased the response to ordinary feeding, probably due to the inhibition of gastric acid secretion and reduction of duodenal acidification. Neurotensin given intra-arterially directly to the pancreas or to isolated intestinal segment increased dose dependently the blood flow and oxygen consumption without affecting general circulation. We conclude that 1) neurotensin mimics the pancreatic secretory effects of intestinal fat, 2) neurotensin may contribute in part to fat-induced stimulation of the pancreatic secretion, and 3) the secretory effects of neurotensin are accompanied by a marked stimulation of intestinal and pancreatic circulation and metabolism.

Human pancreatic secretion and intestinal motility: effects of ileal nutrient perfusion

1990 ◽  
Vol 258 (2) ◽  
pp. G196-G201 ◽  
Author(s):  
P. Layer ◽  
S. Peschel ◽  
T. Schlesinger ◽  
H. Goebell
Keyword(s):  
Pancreatic Secretion ◽  
Intestinal Motility ◽  
Healthy Subjects ◽  
Pancreatic Enzyme ◽  
Essential Amino Acids ◽  
Enzyme Secretion ◽  
Duodenal Juice ◽  
Distal Small Intestine ◽  
Pancreatic Enzyme Secretion ◽  
Stimulation Of

To study the effects of intraileal nutrients on human pancreatic secretion and gastrointestinal motility, nine healthy subjects were intubated with an oroileal multilumen tube for ileal perfusion, duodenal juice aspiration, and intestinal motility recording. The duodenum was perfused continuously with essential amino acids to induce submaximal stimulation of pancreatic enzyme secretion and fed motility pattern. Additional ileal perfusion with carbohydrate at quantities similar to those observed under physiological late postprandial conditions or fat at isocaloric loads significantly decreased pancreatic enzyme outputs by greater than 80% (P less than 0.001) compared with saline. Ileal carbohydrate or fat induced a duodenal motor activity front that migrated distally and was followed by reduced motility. In summary, ileal delivery of small quantities of nutrient markedly decreased endogenously stimulated pancreatic enzyme secretion in humans. This was associated with specific changes in fed intestinal motility that converted to patterns characteristic of the interdigestive state. Our findings suggest that the distal small intestine may participate in the late postprandial regulation of gastrointestinal function in humans.

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

1987 ◽  
Vol 252 (1) ◽  
pp. G8-G12 ◽  
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)

CHANGES OF INTESTINAL MOTILITY AFTER SMALL BOWEL TRANSPLANTATION IN THE RAT

1994 ◽  
Vol 57 (8) ◽  
pp. 1149-1152 ◽  
Author(s):  
Hiromitsu Ishii ◽  
Masato Kusunoki ◽  
Shinsuke Fujita ◽  
Takehira Yamamura ◽  
Joji Utsunomiya
Keyword(s):  
Small Bowel ◽  
Intestinal Motility ◽  
Small Bowel Transplantation

Small intestinal motility in fasted and postprandial states: effect of transient vagosympathetic blockade

1987 ◽  
Vol 252 (3) ◽  
pp. G301-G308 ◽  
Author(s):  
S. A. Chung ◽  
N. E. Diamant
Keyword(s):  
Small Bowel ◽  
Intestinal Motility ◽  
Gastric Fundus ◽  
Phase Iii ◽  
Entire Small Bowel ◽  
Vagal Blockade ◽  
Small Intestinal Motility ◽  
Proximal Small Bowel ◽  
Small Intestinal ◽  
Gastric Contractions

We investigated vagal control of the migrating myoelectric complex (MMC) and postprandial pattern of the canine small intestine. Gastric and small intestinal motility were monitored in six conscious dogs. The vagosympathetic nerves, previously isolated in bilateral skin loops, were blocked by cooling. To feed, a meat-based liquid food was infused by tube into the gastric fundus. MMC phases I, II, III, and IV were observed in the fasted state. On feeding, the fed pattern appeared quickly in the proximal small bowel but was delayed distally. Vagal blockade abolished all gastric contractions and spiking activity as well as the small bowel fed pattern. During vagal blockade, the small bowel exhibited MMC-like migrating bursts of spikes in both the fasted and fed states. The migration and cycling of these bursts were not significantly different from the MMC, but the duodenal and jejunal phase II was absent or shortened. On termination of vagal blockade, normal fasting or fed activity reappeared but with a delay in the fed pattern distally. We conclude: the ileum is the least sensitive to vagal blockade; the fasting vagal influence is exerted primarily on phases I and II of the duodenal and jejunal MMC; the fed pattern throughout the entire small bowel is normally dependent upon vagal integrity; the phase III-like bursts of activity seen during vagal blockade likely represents the intrinsic small bowel MMC, which is vagally independent.

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

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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