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

1977 ◽  
Vol 232 (1) ◽  
pp. E44
Author(s):  
A K Mukhopadhyay ◽  
P J Thor ◽  
E M Copeland ◽  
L R Johnson ◽  
N W Weisbrodt

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.

1986 ◽  
Vol 250 (2) ◽  
pp. G149-G154
Author(s):  
E. Schippers ◽  
J. Janssens ◽  
G. Vantrappen ◽  
M. Vandeweerd ◽  
T. L. Peeters

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.


1985 ◽  
Vol 249 (1) ◽  
pp. G92-G99 ◽  
Author(s):  
J. J. Galligan ◽  
M. Costa ◽  
J. B. Furness

Myoelectric activity was recorded from the gastric antrum and small intestine of conscious, unrestrained guinea pigs using bipolar Ag-Ag chloride electrodes that had been previously implanted under pentobarbital sodium/Innovar anesthesia. In fasted guinea pigs, the migrating myoelectric complex (MMC) was recorded from the small intestine and was observed to propagate aborally at a speed that declined with distance from the pylorus (range of speeds of the front of phase 3: 17.5 cm/min in the duodenum to 4.1 cm/min in the ileum). The complex was not disrupted by feeding but occurred less frequently in the freely fed state (82-min cycle period in the fasted state versus 139 min in the fed state). The complex started in the duodenum and was accompanied by a brief (6.3 +/- 0.9 min) period of inhibition of antral myoelectric activity. Slow waves were also recorded from the gastric antrum (10.3 +/- 1.3/min) and the small intestine. The frequency of intestinal slow waves was uniform along the length of the bowel (26.2 +/- 1.3/min in the duodenum to 24.7 +/- 1.3/min in the ileum). It is concluded that the guinea pig is similar to other mammalian species, so far examined, in its pattern of gastrointestinal myoelectric activity.


1978 ◽  
Vol 56 (4) ◽  
pp. 617-623 ◽  
Author(s):  
Darlene G. Kelly ◽  
Charles F. Code

The study was designed to determine whether the special Na+–H+ barrier function or the gastric mucosa is present in the mucosa of the small bowel and whether a gastric mucosal barrier breaker (hexanoic acid) would accelerate the fluxes of sodium in duodenum–jejunum and ileum as in the stomach. The observations were made in healthy conscious dogs with Thiry-Vella fistulae of the small bowel or Heidenhain pouches of the gastric corpus. These barrier characteristics of the stomach were completely absent in the small intestine where bidirectional Na fluxes were 5–10 times greater than in the stomach and were not accelerated by hexanoic acid as they were in the stomach.A comparison was made between the rates of absorption of hexanoic acid, sodium hexanoate, and HCl from the pouches and fistulae. The lipid-soluble fatty acid was transported at all sites more rapidly than its water-soluble sodium salt. In the stomach and ileum the H+ of HCl and sodium hexanoate were absorbed at similar slow rates. The duodenal–jejunal mucosa, however, transported H+ at rates nearly identical to those of hexanoic acid. In our tests HCl was not neutralized in duodenal contents while large quantities were neutralized in the contents of ileum.


1992 ◽  
Vol 263 (2) ◽  
pp. G248-G253 ◽  
Author(s):  
M. E. Zenilman ◽  
J. E. Parodi ◽  
J. M. Becker

The cyclic nature and distal propagation of the fasting migrating motor complex (MMC) of the small intestine have been well described. The fate of the MMC after feeding, however, has not been elucidated. We used time series analysis with fast Fourier transforms (FFT) to study myoelectric cycling before and after feeding. Ten rats were chronically prepared with bipolar electrodes secured to the duodenum and proximal jejunum. Spikeburst frequency was recorded before and after feeding simple nutrients. During fasting, cyclic activity occurred at the MMC frequency. Although after feeding this periodicity appeared disrupted, FFT analysis showed persistent cycling at the fasted (MMC) rate. Digital filtering of data at the MMC frequency isolated cycling from background noise during both fasted and fed states and showed a depression in the amplitude of the waveform after feeding. Root-mean-square analysis of the waveform confirmed statistically significant depression of amplitude by 47-57%. The waveform propagated from the duodenum to the jejunum during both the fasted and fed state at an unchanged rate. We conclude that factors controlling myoelectric cycling during the fasted state persist after feeding, allowing continued net abroad propulsion of food.


1990 ◽  
Vol 259 (2) ◽  
pp. G226-G232
Author(s):  
C. T. Frantzides ◽  
R. E. Condon ◽  
B. T. Doumas ◽  
J. C. Garancis

In this study, we investigated the role of intrinsic nerves of the small intestine on phase III migration of the migrating myoelectric complex. Fasting myoelectric activity was recorded from the small bowel in chronically instrumented dogs. Once control experiments were completed, the animals were divided into two groups and were reoperated. In the first group of five dogs, a 1.5-g/dl aqueous solution of cobaltous chloride (shown to induce degeneration of intestinal intrinsic nerves) was infused close intra-arterially to perfuse a 15-cm segment of jejunum. In the second group of dogs, a catheter was implanted in a branch of the superior mesenteric artery supplying a 15-cm segment of intestine. Tetrodotoxin (0.3-1 micrograms/kg) was infused through the catheter just before the arrival of phase III activity in the perfused segment. Subsequent to the fifth postcobalt perfusion day, phase III traversed but did not occur in the cobalt-treated segment. When tetrodotoxin was injected through the catheter, spontaneous phasic myoelectric and contractile activities in the perfused jejunal segment were inhibited, but phase III migration was not blocked. These findings suggest 1) acute or chronic defunctioning of enteric nerves does not interrupt phase III migration, but 2) phase III expression is dependent on the integrity of intrinsic nerves.


1992 ◽  
Vol 262 (3) ◽  
pp. G498-G504 ◽  
Author(s):  
M. H. Clench ◽  
J. R. Mathias

The rhythmic oscillating complex (ROC) is described from a series of experiments that surveyed the myoelectric activity of the avian small intestine as recorded from chronically implanted bipolar electrodes. A highly organized myoelectric event in the fasting avian small intestine, the ROC is demonstrated in detail in chickens (Gallus); it is also found in other gallinaceous birds but not in owls (Strix) or mammals. The ROC comprises rapidly propagating bursts of spike potentials (SPBs) that occur in a regular and predictable pattern: single orad SPBs alternate with groups of aborad SPBs. An average ROC in a chicken contains a mean of 78.9 +/- 2.0 (mean +/- SE) SPBs (37% orad, 63% aborad) that rapidly traverse the full length of the small intestine. The aborad SPBs move at mean velocities of 25.0 +/- 0.5 cm/s and last a mean of 0.9 +/- 0.0 s at an electrode site; the orad SPBs are faster (41.2 +/- 2.3 cm/s) and longer in duration (1.3 +/- 0.0 s). ROC activity continues for a mean of 7.6 +/- 0.2 min. ROCs occur only in a well-fasted gut as often as every 3 h and apparently for as long as the bird remains without food. Because ROCs restimulate fed-state activity in the stomach and small intestine, we hypothesize that they recycle nutritive material for further digestive activity in the distal tract.


1975 ◽  
Vol 228 (2) ◽  
pp. 650-654 ◽  
Author(s):  
NW Weisbrodt ◽  
EM Copeland ◽  
EP Moore ◽  
RW Kearley ◽  
LR Johnson

The effect of bilateral thoracic vagotomy on the myoelectric activity of the small intestine was determined in conscious dogs. Animals were implanted with electrodes spaced 25 cm apart along the serosal surface of the small intestine, and a cannula was placed in the most dependent portion of the stomach. Recordings were made with dogs in the fasted and fed states. Two distinct patterns of myoelectric activity were recorded: one typical of the fasted state (the interdigestive myoelectric complex) and one typical of the fed state. After completion of the control recording periods, a truncal vagotomy was performed on each animal. Completeness of vagotomy was confirmed by lack of a gastric secretory response to insulin. Gastric stasis occurred after vagotomy; therefore, the animals' stomachs were emptied via the gastric cannula to obtain a fasted condition. Vagotomy had little to no effect on the fasted pattern of myoelectric activity. The fed pattern was significantly altered in two of the three animals. This alteration could be due to the effect of vagotomy on gastrin release. We conclude that nervous pathways within the vagus may exert some influence on intestinal myoelectric activity but that other neural-humoral pathways are probably involved.


2003 ◽  
Vol 285 (4) ◽  
pp. G688-G695 ◽  
Author(s):  
M. Ehrström ◽  
E. Näslund ◽  
J. Ma ◽  
A. L. Kirchgessner ◽  
P. M. Hellström

Orexin A (OXA)-positive neurons are found in the lateral hypothalamic area and the enteric nervous system. The aim of this study was to investigate the mechanism of OXA action on small bowel motility. Electrodes were implanted in the serosa of the rat small intestine for recordings of myoelectric activity during infusion of saline or OXA in naive rats, vagotomized rats, rats pretreated with guanethidine (3 mg/kg) or Nω-nitro-l-arginine (l-NNA; 1 mg/kg). Naive rats were given a bolus of the orexin receptor-1 (OX1R) antagonist (SB-334867-A; 10 mg/kg), and the effect of both OXA and SB-334867-A on fasting motility was studied. Double-label immunocytochemistry with primary antibodies against OXA, neuronal nitric oxide synthase (nNOS), and OX1R was performed. OXA induced a dose-dependent prolongation of the cycle length of the migrating myoelectric complex (MMC) and, in the higher doses, replaced the activity fronts with an irregular spiking pattern. Vagotomy or pretreatment with guanethidine failed to prevent the response to OXA. The OXA-induced effect on the MMC cycle length was completely inhibited by pretreatment with l-NNA ( P < 0.05), as did SB-334867-A. The OX1R antagonist shortened the MMC cycle length from 14.1 (12.0–23.5) to 11.0 (9.5–14.7) min ( P < 0.05) during control and treatment periods, respectively. Colocalization of OXA and nNOS was observed in myenteric neurons of the duodenum and nerve fibers in the circular muscle. Our results indicate that OXA inhibition of the MMC involves the OX1R and that activation of a l-arginine/NO pathway possibly originating from OX1R/nNOS-containing neurons in the myenteric plexus may mediate this effect. Endogenous OXA may have a physiological role in regulating the MMC.


1999 ◽  
Vol 81 (04) ◽  
pp. 594-560 ◽  
Author(s):  
Florence Ganné ◽  
Marc Vasse ◽  
Jean-Louis Beaudeu ◽  
Jacqueline Peynet ◽  
Arnaud François ◽  
...  

SummaryMonocyte-derived foam cells figure prominently in rupture-prone regions of atherosclerotic plaque. As urokinase/urokinase-receptor (u-PA/u-PAR) is the trigger of a proteolytic cascade responsible for ECM degradation, we have examined the effect of atherogenic lipoproteins on monocyte surface expression of u-PAR and u-PA. Peripheral blood monocytes, isolated from 10 healthy volunteers, were incubated with 10 to 200 µg/ml of native or oxidised (ox-) atherogenous lipoproteins for 18 h and cell surface expression of u-PA and u-PAR was analysed by flow cytometry. Both LDL and Lp(a) induced a dose-dependent increase in u-PA (1.6-fold increase with 200 μg/ml of ox-LDL) and u-PAR [1.7-fold increase with 200 μg/ml of ox-Lp(a)]. There is a great variability of the response among the donors, some of them remaining non-responders (absence of increase of u-PA or u-PAR) even at 200 μg/ml of lipoproteins. In positive responders, enhanced u-PA/u-PAR is associated with a significant increase of plasmin generation (1.9-fold increase with 200 μg/ml of ox-LDL), as determined by an amidolytic assay. Furthermore, monocyte adhesion to vitronectin and fibrinogen was significantly enhanced by the lipoproteins [respectively 2-fold and 1.7-fold increase with 200 μg/ml of ox-Lp(a)], due to the increase of u-PAR and ICAM-1, which are receptors for vitronectin and fibrinogen. These data suggest that atherogenous lipoproteins could contribute to the development of atheromatous plaque by increasing monocyte adhesion and trigger plaque weakening by inducing ECM degradation.


1974 ◽  
Vol 75 (3) ◽  
pp. 428-434 ◽  
Author(s):  
P.-J. Czygan ◽  
M. Breckwoldt ◽  
F. Lehmann ◽  
R. Langefeld ◽  
G. Bettendorf

ABSTRACT The effect of synthetic LH-RH was studied in 100 patients with various types of ovarian insufficiency by following up the FSH- and LH-levels in plasma. LH-RH was administered in doses of 12.5, 25 and 100 μg as a rapid intravenous injection. The patients were classified according to the endocrine state of the pituitary as evidenced by the urinary gonadotrophin levels. A clear correlation between the functional state of the pituitary and its responsiveness to exogenous LH-RH was demonstrated. Most of the patients with undetectable low urinary gonadotrophin levels failed to respond. The majority of patients with gonadotrophin excretion in the normal range and those with elevated levels reacted with a dose dependent increase in circulating LH. The amount of liberated FSH however was related to the injected dose only in patients with high gonadotrophic excretion. The present study indicates that synthetic LH-RH provides a useful tool in the evaluation of the pitutiary function particularly in patients with low and with undetectable gonadotrophin excretion. The data presented in this paper also demonstrate that the functional state of the pituitary is clearly reflected by the urinary gonadotrophin levels.


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