Equine duodenal motility, assessed by ultrasonography, as a predictor of reflux and survival following colic surgery

2019 ◽  
Author(s):  
A. L. Lawson ◽  
C. E. Sherlock ◽  
T. S. Mair
Keyword(s):  
Duodenal Motility

Influence of motilin and cholecystokinin on sphincter of Oddi and duodenal mobility

1987 ◽  
Vol 253 (5) ◽  
pp. G679-G683 ◽  
Author(s):  
E. L. Muller ◽  
P. A. Grace ◽  
R. L. Conter ◽  
J. J. Roslyn ◽  
H. A. Pitt
Keyword(s):  
Sphincter Of Oddi ◽  
Prairie Dogs ◽  
Prairie Dog ◽  
Cholecystokinin Octapeptide ◽  
Side Hole ◽  
Hole Pressure ◽  
Duodenal Motility ◽  
Sphincter Of Oddi Motility ◽  
Duodenal Lumen ◽  
Distal Port

The sphincter of Oddi and the duodenum exhibit cyclical activity in phase with the migrating myoelectric complex. Both motilin and cholecystokinin have been shown to modulate gastrointestinal and sphincter of Oddi motility. However, previous studies have not monitored the effects of these hormones on simultaneously recorded sphincter of Oddi and duodenum pressures. The present investigation was undertaken, therefore, to determine the influence of both motilin and cholecystokinin on simultaneously recorded sphincter of Oddi and duodenal motility. In seven anesthetized prairie dogs, a triple-lumen, side-hole, pressure-monitored perfusion catheter was positioned with the proximal port in the sphincter of Oddi and the distal port in the duodenal lumen. Sphincter of Oddi and duodenal motility was recorded before and during 20-min infusions of motilin and cholecystokinin octapeptide (CCK-8) at 1, 10, and 100 ng.kg-1.min-1. Both hormones produced dose-related increases in sphincter of Oddi and duodenal motility. No response was observed with either hormone at 1 ng.kg-1.min-1. At 10 ng.kg-1.min-1, the duodenum was slightly more sensitive to motilin than to CCK-8, while the sphincter of Oddi was equally affected by both hormones. At 100 ng.kg-1.min-1, both hormones stimulated the sphincter of Oddi and the duodenum equally. These data indicate that in the prairie dog, both motilin and cholecystokinin stimulate sphincter of Oddi and duodenal motility.

Effects of metoclopramide on duodenal motility and flow events, glucose absorption, and incretin hormone release in response to intraduodenal glucose infusion

2010 ◽  
Vol 299 (6) ◽  
pp. G1326-G1333 ◽  
Author(s):  
Paul Kuo ◽  
Max Bellon ◽  
Judith Wishart ◽  
André J. Smout ◽  
Richard H. Holloway ◽  
...  
Keyword(s):  
Blood Glucose Concentration ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Glucose Absorption ◽  
Glucose Infusion ◽  
Pressure Waves ◽  
Incretin Hormone ◽  
Duodenal Motility ◽  
Glucagon Like Peptide 1 ◽  
Gip Release

The contribution of small intestinal motor activity to nutrient absorption is poorly defined. A reduction in duodenal flow events after hyoscine butylbromide, despite no change in pressure waves, was associated with reduced secretion of the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) and a delay in glucose absorption. The aim of this study was to investigate the effect of metoclopramide on duodenal motility and flow events, incretin hormone secretion, and glucose absorption. Eight healthy volunteers (7 males and 1 female; age 29.8 ± 4.6 yr; body mass index 24.5 ± 0.9 kg/m2) were studied two times in randomized order. A combined manometry and impedance catheter was used to measure pressure waves and flow events in the same region of the duodenum simultaneously. Metoclopramide (10 mg) or control was administered intravenously as a bolus, followed by an intraduodenal glucose infusion for 60 min (3 kcal/min) incorporating the14C-labeled glucose analog 3- O-methylglucose (3-OMG). We found that metoclopramide was associated with more duodenal pressure waves and propagated pressure sequences than control ( P < 0.05 for both) during intraduodenal glucose infusion. However, the number of duodenal flow events, blood glucose concentration, and plasma 3-[14C]OMG activity did not differ between the two study days. Metoclopramide was associated with increased plasma concentrations of GLP-1 ( P < 0.05) and GIP ( P = 0.07) but lower plasma insulin concentrations ( P < 0.05). We concluded that metoclopramide was associated with increased frequency of duodenal pressure waves but no change in duodenal flow events and glucose absorption. Furthermore, GLP-1 and GIP release increased with metoclopramide, but insulin release paradoxically decreased.

Relationship of plasma motilin concentration to fat ingestion, duodenal acidification and alkalinization, and migrating motor complexes in dogs

1981 ◽  
Vol 59 (2) ◽  
pp. 180-187 ◽  
Author(s):  
J. E. T. Fox ◽  
N. S. Track ◽  
E. E. Daniel
Keyword(s):  
Species Difference ◽  
Maximal Activity ◽  
Significant Rise ◽  
Migrating Motor Complex ◽  
Phase Iii ◽  
Complex Activity ◽  
Duodenal Motility ◽  
Motor Complex ◽  
Duodenal Acidification ◽  
Plasma Motilin

Plasma motilin concentrations were measured in dogs following duodenal acidification and alkalinization and gastric instillation of fat. Antral and duodenal motility were recorded concurrently using intraluminal manometry. Alkalinization of the duodenum produced an increase in antral and duodenal motility and a significant rise in plasma motilin. Alkaline infusions at 5 mL/min into the duodenum initiated phase III of a migrating motor complex both in the antrum and in the duodenum. Duodenal acid infusions produced no change in plasma motilin concentrations while inhibiting antral motility and stimulating duodenal motility for the duration of the infusion. Gastric instillation of 60 g fat produced a 25% increase above basal motilin levels at 50 min after instillation. Motilin levels monitored during spontaneous migrating motor complexes showed peak motilin levels occurring during maximal activity of the antral duodenal region in seven out of nine motor complexes examined but motilin peaks also occurred without migrating complexes being present in this area and, as well, complexes occurred when motilin was undetectable. These results taken together with our other studies in man confirm that a true species difference exists between man and dog in the hormonal motor response to duodenal alkalinization. Although a relationship appears to exist between the appearance of maximal migrating motor complex activity in the gastroduodenal area and plasma motilin concentrations in dogs as in humans, the motilin peaks are probably neither necessary nor sufficient to induce phase III activity.

Erythromycin Elicits Opposite Effects on Antro-Bulbar and Duodenal Motility: Analysis in Diabetics by Cineradiography

1997 ◽  
Vol 105 (6) ◽  
pp. 591-595 ◽  
Author(s):  
M Boiron ◽  
E Dorval ◽  
E.H Metman ◽  
D Alison ◽  
L Gameiro ◽  
...  
Keyword(s):  
Duodenal Motility

Stimulation of duodenal motility by hyperosmolar mannitol depends on local osmoreceptor control

1994 ◽  
Vol 266 (5) ◽  
pp. G940-G943 ◽  
Author(s):  
H. C. Lin ◽  
J. D. Elashoff ◽  
G. M. Kwok ◽  
Y. G. Gu ◽  
J. H. Meyer
Keyword(s):  
Intestinal Motility ◽  
Control Mechanism ◽  
Experimental Methods ◽  
Dose Effect ◽  
Duodenal Motility ◽  
Significant Difference ◽  
Intestinal Distension ◽  
Osmotic Equilibration ◽  
Spike Bursts ◽  
Stimulation Of

Duodenal motility is stimulated by hyperosmolar solution. Since intestinal distension also stimulates intestinal motility, this increase in the motility response may be due to either stimulation of duodenal local osmoreceptor control or intestinal distension resulting from osmotic equilibration. To test which mechanism is primarily responsible for this osmotically sensitive effect, we compared the number of duodenal spike bursts in five dogs equipped with duodenal fistulas that allowed for the preservation or removal of intestinal distension. The response to 300 vs. 1,200 mosM mannitol was compared under three experimental perfusion methods: 1) distension was preserved both proximal and distal to the fistula (DD); 2) distension proximal to the fistula was removed (rD); and 3) distension both proximal and distal to the fistula was removed (rr). The test solutions had access to either the whole gut (DD and rD) or only the first 10 cm of the duodenum (rr). We found that 1) there were more spike bursts after the hyperosmolar solution (dose effect, P < 0.05, analysis of variance); 2) there was no significant difference between the three experimental methods; and 3) the stimulating effect of hyperosmolar solution depended on the first 10 cm of the duodenum. Thus, since hyperosmolar solution increased duodenal motility regardless of whether intestinal distension was preserved or removed, the stimulating effect of hyperosmolar solution on duodenal motility was primarily the result of a local osmoreceptor control mechanism located in the first 10 cm of the duodenum.

Relation between duodenal alkaline secretion and motility in fasted and sham-fed dogs

1986 ◽  
Vol 251 (5) ◽  
pp. G591-G596 ◽  
Author(s):  
S. J. Konturek ◽  
P. Thor
Keyword(s):  
Motor Activity ◽  
Vagal Stimulation ◽  
Secretory Activity ◽  
Phase Iii ◽  
Plasma Gastrin ◽  
Marked Rise ◽  
Sham Feeding ◽  
Duodenal Motility ◽  
Alkaline Secretion ◽  
Stimulation Of

A relation between duodenal myoelectric and motor activity and alkaline secretion has been investigated in conscious dogs under basal conditions and following vagal excitation with and without pretreatment with atropine or indomethacin. It was found that duodenal alkaline secretion shows typical periodicity in phase with the myoelectric or motor activity of the duodenum, reaching a peak during phase III and a nadir during phase I of the migrating motor complex (MMC). Sham feeding interrupted the motor and secretory MMC cycle and caused a prolonged increase in duodenal myoelectric or motor activity as well as a sudden and marked rise in duodenal alkaline secretion accompanied by a significant elevation in plasma gastrin and pancreatic polypeptide. Atropine and indomethacin abolished the motor and secretory duodenal cycles and reduced basal alkaline secretion significantly. Atropine abolished, whereas indomethacin increased duodenal myoelectric or motor activity during basal conditions and after vagal stimulation. Neither atropine nor indomethacin abolished sham feeding-induced duodenal alkaline secretion. We conclude that duodenal alkaline secretion fluctuates cyclically in phase with duodenal motility, vagal excitation results in a potent stimulation of duodenal motor and secretory activity, and the mechanism of vagally induced duodenal alkaline secretion is only partly cholinergic and does not involve endogenous generation of prostaglandins.

The Physiologic Interpretation of Duodenal Motility

Radiology ◽  
1933 ◽  
Vol 21 (4) ◽  
pp. 337-347
Author(s):  
N. S. Zeitlin
Keyword(s):  
Duodenal Motility

Interaction between prostanoids, NO, and VIP in modulation of duodenal alkaline secretion and motility

1996 ◽  
Vol 271 (4) ◽  
pp. G582-G590 ◽  
Author(s):  
M. Sababi ◽  
A. Hallgren ◽  
O. Nylander
Keyword(s):  
Smooth Muscle ◽  
Methyl Ester ◽  
Inhibitory Action ◽  
Muscle Relaxation ◽  
Intraluminal Pressure ◽  
Smooth Muscle Relaxation ◽  
Pressure Measurements ◽  
Stimulatory Action ◽  
Duodenal Motility ◽  
Alkaline Secretion

The relation between duodenal motility and duodenal mucosal alkaline secretion (DMAS) was examined in anesthetized rats. The duodenum was perfused with saline, and DMAS was determined by titration. Duodenal motility, assessed by intraluminal pressure measurements, was induced by indomethacin and/or N omega-nitro-L-arginine methyl ester (L-NAME) and inhibited by iloprost or vasoactive intestinal peptide (VIP). Six of 66 rats showed spontaneous duodenal contractions. Basal DMAS was higher in these rats than in those without contractions. Rats treated with indomethacin and L-NAME before abdominal operation exhibited duodenal motility postoperatively and had higher DMAS than in controls. Iloprost abolished both the duodenal motility increase and increase in DMAS induced by indomethacin. L-NAME-induced motility and increase in DMAS were antagonized by L-arginine. VIP increased DMAS without affecting motility. VIP abolished indomethacin-induced motility and augmented indomethacin-stimulated DMAS. VIP reduced L-NAME-induced motility and slightly increased L-NAME-stimulated DMAS. It is concluded that DMAS varies with duodenal motility. Prostaglandins and NO inhibit duodenal motility, thereby indirectly reducing DMAS. VIP may have dual effects on DMAS, an inhibitory action mediated via smooth muscle relaxation and a stimulatory action independent of motility.

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