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.

Stimulation of growth of a colon cancer cell line by gastrin

1986 ◽  
Vol 251 (5) ◽  
pp. G597-G601 ◽  
Author(s):  
C. J. Kusyk ◽  
N. O. McNiel ◽  
L. R. Johnson
Keyword(s):  
Motor Activity ◽  
Cancer Cell Line ◽  
Secretory Activity ◽  
Colon Cancer Cell Line ◽  
Phase Iii ◽  
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.

Cephalic phase of gastroduodenal alkaline secretion

1987 ◽  
Vol 252 (6) ◽  
pp. G742-G747 ◽  
Author(s):  
S. J. Konturek ◽  
P. Thor ◽  
J. Bilski ◽  
J. Tasler ◽  
M. Cieszkowski
Keyword(s):  
Significant Influence ◽  
Vagal Stimulation ◽  
Conscious Dogs ◽  
Insulin Hypoglycemia ◽  
Sham Feeding ◽  
Cephalic Phase ◽  
Alkaline Secretion ◽  
Stimulation Of

Alkaline secretion measured under basal conditions in the intact stomach of conscious dogs averaged 47 mumol/30 min and was about twice lower than that recorded in the proximal (approximately 7 cm long) portion of the duodenum. Vagal excitation elicited by sham feeding and insulin resulted in a marked stimulation of alkaline secretion both from the stomach and the duodenum. Atropine significantly reduced gastric and duodenal alkaline secretion under basal state. It abolished gastric and diminished duodenal alkaline response to sham feeding and insulin hypoglycemia, while propranolol was without significant influence. Indomethacin reduced by approximately 75% basal duodenal alkaline secretion but did not prevent the increment in alkaline response to vagal stimulation. We postulate the existence of the cephalic phase of gastroduodenal alkaline secretion, which seems to be cholinergically dependent in the stomach and partly of noncholinergic and nonadrenergic character but prostaglandin dependent in the duodenum.

Obestatin inhibits motor activity in the antrum and duodenum in the fed state of conscious rats

2008 ◽  
Vol 294 (5) ◽  
pp. G1210-G1218 ◽  
Author(s):  
Koji Ataka ◽  
Akio Inui ◽  
Akihiro Asakawa ◽  
Ikuo Kato ◽  
Mineko Fujimiya
Keyword(s):  
Motor Activity ◽  
Immunohistochemical Analysis ◽  
Phase Iii ◽  
Fed State ◽  
Conscious Rats ◽  
Duodenal Motility ◽  
Gastroduodenal Motility ◽  
The Brain

Obestatin is a novel peptide encoded by the ghrelin precursor gene; however, its effects on gastrointestinal motility remain controversial. Here we have examined the effects of obestatin on fed and fasted motor activities in the stomach and duodenum of freely moving conscious rats. We examined the effects of intravenous (IV) injection of obestatin on the percentage motor index (%MI) and phase III-like contractions in the antrum and duodenum. The brain mechanism mediating the action of obestatin on gastroduodenal motility and the involvement of vagal afferent pathway were also examined. Between 30 and 90 min after IV injection, obestatin decreased the %MI in the antrum and prolonged the time taken to return to fasted motility in the duodenum in fed rats given 3 g of chow after 18 h of fasting. Immunohistochemical analysis demonstrated that corticotropin-releasing factor- and urocortin-2-containing neurons in the paraventricular nucleus in the hypothalamus were activated by IV injection of obestatin. Intracerebroventricular injection of CRF type 1 and type 2 receptor antagonists prevented the effects of obestatin on gastroduodenal motility. Capsaicin treatment blocked the effects of obestatin on duodenal motility but not on antral motility. Obestatin failed to antagonize ghrelin-induced stimulation of gastroduodenal motility. These results suggest that, in the fed state, obestatin inhibits motor activity in the antrum and duodenum and that CRF type 1 and type 2 receptors in the brain might be involved in these effects of obestatin on gastroduodenal motility.

Effects of antral vagotomy in dogs on gastrin and gastric secretion with various stimuli

1990 ◽  
Vol 258 (6) ◽  
pp. G919-G925 ◽  
Author(s):  
B. I. Hirschowitz ◽  
J. Fong
Keyword(s):  
Gastric Secretion ◽  
Serum Gastrin ◽  
Vagal Stimulation ◽  
Gastric Fistula ◽  
Gastrin Release ◽  
Cholinergic Stimulation ◽  
Sham Feeding ◽  
Human Gastrin ◽  
Cholinergic Effects ◽  
Stimulation Of

In four gastric-fistula dogs, selective antral vagotomy markedly reduced the vagal stimulation of gastrin release, thereby defining both the vagal pathway for stimulation of gastrin and the anatomic source of such gastrin release. Despite loss of gastrin response, vagal excitation by 100 mg/kg 2-deoxy-D-glucose (2-DG) produced the same acid and pepsin responses after antral vagotomy as before, but there was an approximately 40% diminished fundic response to pentagastrin, histamine, and synthetic human gastrin, as well as to endogenous gastrin released by graded doses of bombesin. Bethanechol did not reverse the defect, ruling out inadvertent fundic vagal denervation, nor did raising serum gastrin by bombesin alter the response to vagal stimulation by 2-DG. Fundic response to bethanechol was increased by approximately 60%, and the output of gastrin increased at least fivefold after antral vagotomy. Gastrin responses to food were diminished and those to sham feeding were eliminated. Separation of the denervated antral pouch had no additional effect on acid secretion. Vagal stimulation of gastric secretion thus occurs almost exclusively through direct cholinergic effects on the fundus with little or no contribution from antral gastrin. Vagal denervation sensitizes the antrum to cholinergic stimulation.

Motilin and the vagus in dogs

1984 ◽  
Vol 62 (9) ◽  
pp. 1092-1096 ◽  
Author(s):  
M. Lemoyne ◽  
R. Wassef ◽  
D. Tassé ◽  
L. Trudel ◽  
P. Poitras
Keyword(s):  
Small Intestine ◽  
Vagal Stimulation ◽  
Phase Iii ◽  
Inhibitory Influence ◽  
Myoelectrical Activity ◽  
Sham Feeding ◽  
Implanted Electrodes ◽  
Motility Pattern ◽  
Before And After ◽  
Circulating Levels

The aim of this work was to determine the influence of the vagus on the circulating levels of immunoreactive (IR) motilin. Five mongrel dogs were equipped with chronically implanted electrodes in the small intestine to record the myoelectrical activity. The release of IR motilin during fasting, after a meal, and during an infusion of insulin was studied before and after truncal vagotomy at the diaphragmatic level. When tested at least two weeks after the operation, the motility pattern of the small intestine and the secretion of IR motilin remained unaltered by vagal section. Cyclic increases in IR motilin associated with phase III's of the interdigestive myoelectric complexes were still observed after vagotomy (maximum levels of IR motilin: 250 ± 37 versus 239 ± 19 fmol∙mL−1, not significant), and they were still abolished by feeding or by insulin. However, an inhibitory influence can probably be mediated by the vagus since, in normal animals, vagal stimulation by a "modified sham feeding" (tease feeding or presentation of food) at the beginning of a period of phase III activity promptly interrupted this part of the complex and decreased significantly the release of IR motilin by about 20%. The release of motilin is not chronically altered by distal vagotomy in dogs.

Gut hormones in stimulation of gastroduodenal alkaline secretion in conscious dogs

1985 ◽  
Vol 248 (6) ◽  
pp. G687-G691 ◽  
Author(s):  
S. J. Konturek ◽  
J. Bilski ◽  
J. Tasler ◽  
J. Laskiewicz
Keyword(s):  
Gut Hormones ◽  
Duodenal Mucosa ◽  
Conscious Dogs ◽  
Significant Elevation ◽  
Plasma Gastrin ◽  
Inhibitory Peptide ◽  
Gastroduodenal Mucosa ◽  
Alkaline Secretion ◽  
Significant Increment ◽  
Stimulation Of

Alkaline secretion from the fundic and antral pouches of the stomach and the loops of proximal and distal duodenum was measured in conscious dogs under basal conditions and after intragastric instillation of HCl solution, meat feeding, or intravenous infusion of various gut hormones. In control tests on fasted dogs HCO-3 output from the duodenal mucosa was severalfold higher than that from the gastric mucosa. Instillation of 10 mM HCl into the stomach resulted in a significant increment in HCO-3 secretion from the gastric pouches and proximal duodenal loops, and this was accompanied by a marked increase in plasma secretin, cholecystokinin (CCK), and pancreatic polypeptide (PP) levels. Meat feeding stimulated HCO-3 secretion from proximal duodenum, and it was accompanied by a significant elevation in plasma gastrin, secretin, CCK, gastric inhibitory peptide, and PP. Among exogenous hormones, the most effective stimulant of HCO-3 secretion was PP, which caused a significant increase in HCO-3 output from the gastric and duodenal mucosa at doses (125-500 pmol X kg-1 X h-1) that raised plasma PP to postprandial levels. CCK in physiological doses (21-85 pmol.kg-.h-1) also stimulated HCO-3 secretion from gastric pouches and proximal duodenal loops. Neurotensin stimulated HCO-3 secretion from both gastric pouches and duodenal loops. In contrast, gastrin or secretin did not affect significantly HCO-3 secretion from the gastroduodenal mucosa. This study provides evidence that some gut hormones, particularly PP, CCK, and neurotensin, may be involved in the physiological stimulation of gastroduodenal alkaline secretion.

Relationships between duodenal motility and pancreatic secretion in fasted and fed dogs

1986 ◽  
Vol 250 (5) ◽  
pp. G570-G574
Author(s):  
S. J. Konturek ◽  
P. J. Thor ◽  
J. Bilski ◽  
W. Bielanski ◽  
J. Laskiewicz
Keyword(s):  
Motor Activity ◽  
Pancreatic Secretion ◽  
Gut Hormones ◽  
Significant Rise ◽  
Phase Iii ◽  
Duodenal Motility ◽  
Gut Hormone ◽  
Plasma Motilin ◽  
Physiological Dose ◽  
Secretory Capacity

A relationship between duodenal myoelectric or motor activity and exocrine pancreatic secretion as well as plasma gut hormone levels has been investigated in fasted dogs, fed dogs, and dogs that were stimulated with exogenous gut hormones. Pancreatic secretion showed typical periodicity in phase with the myoelectric or motor activity of the duodenum. Fasting pancreatic bicarbonate and protein secretion reached peaks during phase III of the interdigestive migrating motor complex (MMC) cycle that were significantly larger than nadir levels occurring during phase I of the cycle. These fasting bicarbonate and protein peaks reached, respectively, approximately 9 and 30% of the highest postprandial outputs and 4 and 14% of the maximal secretory capacity elicited by secretin or CCK. They were accompanied by a significant rise in plasma motilin, gastrin, and pancreatic polypeptide (PP), but only exogenous motilin given in physiological dose induced motility pattern and pancreatic secretion similar to those observed during phase III. Feeding interrupted both motor and secretory MMC cycle, increased the pancreatic secretion to approximately 40-60% of the maximal secretory capacity, and was accompanied by increments in plasma gastrin, cholecystokinin (CCK), secretin, and PP. None of these hormones applied alone in physiological dose was capable of reproducing the postprandial inhibition of MMC cycles. We conclude that the pancreatic secretion in fasted dogs fluctuates periodically in phase with duodenal motility, but the phase III peak secretory outputs represent only minute fractions of the maximal secretory capacity and can therefore be ignored in regular testing of pancreatic secretion.

Prolonged Apnea, Vagal Overactivity, and Sudden Infant Death

PEDIATRICS ◽  
1973 ◽  
Vol 51 (4) ◽  
pp. 755-755
Author(s):  
David S. Bachman
Keyword(s):  
At Risk ◽  
Vagus Nerve ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Vagal Stimulation ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Prolonged Apnea ◽  
Stimulation Of

The article on prolonged apnea and the sudden infant death syndrome (SIDS) by Steinschneider1 is very exciting in that it suggests the possibility of identifying infants at risk from SIDS before the final event. Obviously, it is of great importance to learn the mechanism causing the preceding apneic episodes. Do they represent vagal overactivity? Stimulation of the intact vagus nerve in the unanesthetized monkey causes apnea, as well as bradycardia and even arrhythmias.2 In fact, we have seen myocardial myocytolysis secondary to vagal stimulation.3

Neural Patterns Associated with Ventilatory Movements in Dragonfly Larvae

1970 ◽  
Vol 52 (1) ◽  
pp. 167-175
Author(s):  
P. J. MILL
Keyword(s):  
Control System ◽  
Motor Activity ◽  
Action Potentials ◽  
Motor Units ◽  
The Other ◽  
Ventilatory Control ◽  
Expiratory Phase ◽  
Segmental Nerve ◽  
Ventral Muscle ◽  
Stimulation Of

1. Rhythmic bursts of motor activity associated with the expiratory phase of ventilation have been recorded from the second lateral segmental nerves of posterior abdominal ganglia in Aeshna and Anax larvae. 2. In Aeshna the rhythmic expiratory bursts contain one, or sometimes two, motor units; whereas in Anax there are almost invariably three units. In both animals only one unit is associated with action potentials in the respiratory dorso-ventral muscle. 3. Motor activity synchronized with the expiratory bursts in the second nerves has been recorded from the other lateral nerves and from the last unpaired nerve. In addition the fifth lateral nerves carry inspiratory bursts. 4. It has been confirmed that stimulation of a first segmental nerve can re-set the ventilatory rhythm by initiating an expiratory burst in the second nerves. The original frequency is immediately resumed on cessation of stimulation. 5. The nature of the ventilatory control system in dragonfly larvae is discussed in relation to other rhythmic systems in the arthropods.

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