Effect of erythromycin on interdigestive gastrointestinal contractile activity and plasma motilin concentration in humans

1993 ◽  
Vol 38 (5) ◽  
pp. 870-876 ◽  
Author(s):  
O. Kawamura ◽  
T. Sekiguchi ◽  
M. Kusano ◽  
T. Nishioka ◽  
Z. Itoh
Keyword(s):  
Contractile Activity ◽  
Plasma Motilin ◽  
Gastrointestinal Contractile Activity

Erythromycin mimics exogenous motilin in gastrointestinal contractile activity in the dog

1984 ◽  
Vol 247 (6) ◽  
pp. G688-G694 ◽  
Author(s):  
Z. Itoh ◽  
M. Nakaya ◽  
T. Suzuki ◽  
H. Arai ◽  
K. Wakabayashi
Keyword(s):  
Small Intestine ◽  
Gastrointestinal Tract ◽  
Intravenous Infusion ◽  
Contractile Activity ◽  
Contractile Force ◽  
Naturally Occurring ◽  
Gastrointestinal Motor ◽  
Plasma Motilin ◽  
Interdigestive Migrating Contractions ◽  
Gastrointestinal Contractile Activity

The gastrointestinal motor stimulating activity of erythromycin (EM) was studied in conscious dogs. It was found that a 20-min intravenous infusion of EM lactobionate at a dose of 50–100 micrograms (potency) X kg-1 X h-1 induced a group of strong contractions in the stomach and the duodenum, and the contractions migrated along the small intestine to the terminal ileum. The EM-induced contractions were quite similar to the naturally occurring interdigestive migrating contractions (IMC) in the gastrointestinal tract in frequency, contractile force, and duration of the contractions, migrating velocity, and accompanying peaks of plasma motilin concentration. The EM-induced contractions in the stomach were inhibited by feeding and intravenous infusion of pentagastrin (1.5 micrograms X kg-1 X h-1) but were not affected by secretin; these findings are identical to those found with the naturally occurring and motilin-induced contractions. Like motilin, EM stimulated motor activity only during the interdigestive state. We conclude that EM induces IMC associated with the release of endogenous motilin in the dog.

Changes in plasma motilin concentration and gastrointestinal contractile activity in conscious dogs

1978 ◽  
Vol 23 (10) ◽  
pp. 929-935 ◽  
Author(s):  
Zen Itoh ◽  
Shinjin Takeuchi ◽  
Isamu Aizawa ◽  
Kohzaburo Mori ◽  
Tomohiko Taminato ◽  
...  
Keyword(s):  
Contractile Activity ◽  
Conscious Dogs ◽  
Plasma Motilin ◽  
Gastrointestinal Contractile Activity

Effects of Motilin and Mitemcinal (GM-611) on Gastrointestinal Contractile Activity in Rhesus Monkeys In Vivo and In Vitro

2007 ◽  
Vol 52 (11) ◽  
pp. 3112-3122 ◽  
Author(s):  
Kenji Yogo ◽  
Ken-ichi Ozaki ◽  
Hisanori Takanashi ◽  
Masao Koto ◽  
Zen Itoh ◽  
...  
Keyword(s):  
Rhesus Monkeys ◽  
Contractile Activity ◽  
Gastrointestinal Contractile Activity

Regulation of plasma motilin by opioids in the dog

1989 ◽  
Vol 257 (1) ◽  
pp. G41-G45
Author(s):  
P. Poitras ◽  
M. Boivin ◽  
R. G. Lahaie ◽  
L. Trudel
Keyword(s):  
Opioid Receptor ◽  
Contractile Activity ◽  
Endogenous Opioids ◽  
Phase Iii ◽  
Endogenous Opiates ◽  
Small Intestinal Motility ◽  
Opioid Administration ◽  
Small Intestinal ◽  
Plasma Motilin ◽  
Opioid Receptor Agonists

In the first part of this study, we compared the effects of morphine and trimebutine, two opioid receptor agonists, on small intestinal motility and plasma motilin in dogs. Morphine (100 micrograms/kg iv for 10 min) induced first a typical vomiting myoelectric profile followed subsequently by a migrating electrical activity mimicking phase III of the migrating myoelectric complex; trimebutine (5 mg/kg iv for 10 min) initiated only a migrating phase III-like activity. Despite their different initial contractile effects, both agents induced a significant and similar rise in plasma motilin that preceded the beginning of the premature phase III. In the second portion of the study, naloxone, an opioid receptor antagonist, was infused to verify the influence of endogenous opiates on plasma motilin and on the migrating motor complex. Naloxone (2 mg/kg, then 0.5 mg.kg-1.h-1 iv) delayed significantly the cyclic recurrence of plasma motilin peak increases and of the phase IIIs. In some animals, where naloxone abolished the phase IIIs, the amplitude of the motilin peak increases was significantly diminished. These results suggest 1) that opioid administration increases plasma levels of motilin by a mechanism that is independent of the intestinal contractile activity, and 2) that endogenous opioids could be physiological inducers of plasma motilin increases in the conscious dog.

The effect of growth hormone releasing peptide-2 on upper gastrointestinal contractile activity and food intake in conscious dogs

2009 ◽  
Vol 44 (4) ◽  
pp. 297-304 ◽  
Author(s):  
Katsuyoshi Kudoh ◽  
Chikashi Shibata ◽  
Yuji Funayama ◽  
Kouhei Fukushima ◽  
Tatsuya Ueno ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Food Intake ◽  
Contractile Activity ◽  
Conscious Dogs ◽  
Gastrointestinal Contractile Activity ◽  
Upper Gastrointestinal

Motilin controls cyclic release of insulin through vagal cholinergic muscarinic pathways in fasted dogs

1998 ◽  
Vol 274 (1) ◽  
pp. G87-G95 ◽  
Author(s):  
Hideki Suzuki ◽  
Erito Mochiki ◽  
Norihiro Haga ◽  
Minoru Satoh ◽  
Akiyoshi Mizumoto ◽  
...  
Keyword(s):  
Insulin Release ◽  
Islet Cells ◽  
Contractile Activity ◽  
Close Association ◽  
Phase Iii ◽  
Force Transducers ◽  
Specific Radioimmunoassay ◽  
Plasma Motilin ◽  
Interdigestive Migrating Contractions ◽  
Perifusion System

The effect of motilin on insulin release has not been studied in the interdigestive state. Adult mongrel dogs were chronically implanted with force transducers in the stomach and duodenum to monitor contractile activity, and the plasma motilin and insulin concentrations were measured by a specific radioimmunoassay and enzyme immunoassay, respectively. The concentration of insulin in plasma was found to fluctuate in close association with that of motilin and phase III of the interdigestive migrating contractions in the stomach. This spontaneous release of insulin was mimicked by intravenous infusion of motilin at a dose of 0.3 μg ⋅ kg−1⋅ h−1. Exogenous motilin (0.01–0.3 μg/kg) dose dependently stimulated insulin release, which was abolished by atropine, hexamethonium, ondansetron, and truncal vagotomy. Phentolamine significantly enhanced, whereas propranolol inhibited, motilin-induced insulin release. In a perifusion system using islet cells from the canine pancreas, motilin did not affect insulin release. In conclusion, motilin stimulates insulin release through vagal cholinergic, muscarinic receptors on pancreatic β-cells, and the effect appears to be modulated by adrenergic nerves.

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