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

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.

1980 ◽  
Vol 238 (1) ◽  
pp. G50-G56
Author(s):  
S. J. Konturek ◽  
R. Siebers

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.


1981 ◽  
Vol 321 (1) ◽  
pp. 483-494 ◽  
Author(s):  
J. da Cunha Melo ◽  
R. W. Summers ◽  
H. H. Thompson ◽  
D. L. Wingate ◽  
R. Yanda

1977 ◽  
Vol 55 (4) ◽  
pp. 958-961 ◽  
Author(s):  
K. Krnjević ◽  
Dušan Lekić

In cats, under Dial anaesthesia, Renshaw cells were excited by microiontophoretic applications of acetylcholine (ACh), aspartate, and glutamate. Substance P, in small doses (10–30 nA), selectively abolished the responses to ACh, leaving the discharges evoked by the amino acids unchanged or enhanced. Higher doses (> 50 nA) depressed all responses, but those evoked by amino acids went down last and recovered sooner. By contrast, neither synaptic responses to ventral root stimulation nor spontaneous discharges were affected by substance P, presumably owing to the high efficacy of synaptic transmission and the presence of diffusion barriers around junctional sites.


1983 ◽  
Vol 244 (2) ◽  
pp. G160-G164
Author(s):  
J. Heppell ◽  
J. M. Becker ◽  
K. A. Kelly ◽  
A. R. Zinsmeister

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.


1988 ◽  
Vol 255 (4) ◽  
pp. G498-G504 ◽  
Author(s):  
P. Thor ◽  
J. Laskiewicz ◽  
P. Konturek ◽  
S. J. Konturek

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.


1987 ◽  
Vol 252 (1) ◽  
pp. G8-G12 ◽  
Author(s):  
P. Thor ◽  
J. Laskiewicz ◽  
J. W. Konturek ◽  
S. J. Konturek ◽  
W. Creutzfeldt

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)


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

1987 ◽  
Vol 252 (3) ◽  
pp. G301-G308 ◽  
Author(s):  
S. A. Chung ◽  
N. E. Diamant

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.


1977 ◽  
Vol 55 (2) ◽  
pp. 234-242 ◽  
Author(s):  
M. Rezek ◽  
V. Havlicek ◽  
L. Leybin ◽  
C. Pinsky ◽  
E. A. Kroeger ◽  
...  

The administration of small doses of somatostatin (SRIF) (0.01 and 0.1 μg) into the neostriatal complex of unrestrained, freely moving rats induced general behavioral excitation associated with a variety of stereotyped movements, tremors, and a reduction of rapid eye movements (REM) and deep slow wave sleep (SWS). In contrast, the higher doses of SRIF (1.0 and 10.0 μg) caused movements to be uncoordinated and frequently induced more severe difficulties in motor control such as contralateral hemiplegia-in-extension which restricted or completely prevented the expression of normal behavioral patterns. As a result, the animals appeared drowsy and inhibited. Analysis of the sleep-waking cycle revealed prolonged periods of a shallow SWS while REM sleep and deep SWS were markedly reduced; electroencephalogram recordings revealed periods of dissociation from behavior. The administration of endocrinologically inactive as well as the active analogues of SRIF failed to induce effects comparable with those observed after the administration of the same dose of the native hormone (10.0 μg).


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