Somatostatin inhibits motilin-induced interdigestive contractile activity in the dog

Ormsbee, Herbert S.; Koehler, Stewart L.; Telford, Gordon L.

doi:10.1007/bf01079786

Cited by 63 publications

(13 citation statements)

References 18 publications

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“…Octreotide is thought to induce motor activity in the intestine via a local mechanism. The absence of a prokinetic effect on the stomach by somatostatin 24 has been reported.…”

Section: Commentsmentioning

confidence: 99%

Amelioration of intestinal dysmotility and stasis by octreotide early after small-bowel autotransplantation in dogs

Nakada

Ikoma

Suzuki

et al. 1995

The American Journal of Surgery

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“…Octreotide is thought to induce motor activity in the intestine via a local mechanism. The absence of a prokinetic effect on the stomach by somatostatin 24 has been reported.…”

Section: Commentsmentioning

confidence: 99%

Amelioration of intestinal dysmotility and stasis by octreotide early after small-bowel autotransplantation in dogs

Nakada

Ikoma

Suzuki

et al. 1995

The American Journal of Surgery

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“…Because MMCs originate in the stomach, a potential for somatostatin's role in regulating their initiation was established by the observation that the periodic peaks in plasma SLI coincided with the gastric phase of MMCs (1). Generally, investigators agree that exogenous infusion of somatostatin inhibits MMCs that are generated in the stomach either naturally (184) or by infusion of motilin (168). On the other hand, MMCs that originate in the intestine appear to be stimulated by somatostatin (142,180,254).…”

Section: Gastrointestinal Motilitymentioning

confidence: 99%

Somatostatin

Yamada¹,

Chiba²

1989

Comprehensive Physiology

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“…In the stomach, somatostatin inhibits the normal occurrence o f cyclic interdigestive and fed motor activities [122], In the intestine, the peptide initiates ectopic fronts under basal conditions but inhibits fed motility [123].…”

Section: Octreotidementioning

confidence: 99%

Pharmacological Stimulation of Gastrointestinal Motility: Where We Are and Where Are We Going?

Scarpignato¹

1997

Dig Dis

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Drugs affecting gastrointestinal motility have become valuable in the management of a number of diseases. Medications that enhance the transit of material through the gastrointestinal tract are called prokinetics. Although symptom improvement can be seen in a variety of motility disorders, these medications have not shown a selective benefit for a particular motility disturbance or symptom complex. This class of drugs includes several subclasses, each with a distinct mechanism of action. Amongst the existing prokinetic compounds, dopamine antagonists, on the one hand, and cholinomimetic drugs, on the other hand, should be distinguished. Since compounds endowed with dopamine antagonism have the disadvantage of causing neuroendocrine side effects and/or extrapyramidal dyskinetic reactions (seen especially after metoclopramide), the recently developed non-cholinergic non-antidopaminergic compound, cisapride, seems to be the most effective one. Its main mechanism of action is considered to be the stimulation of myenteric cholinergic nerves with consequent increase of acetylcholine release. Recent evidence suggests that blockade of CCK receptors and stimulation of motilin receptors are also promising avenues to increase gastrointestinal motility. Since drugs acting on 5-HT receptors are presently the best available motor-stimulating compounds, new derivatives are being developed as gastrokinetic drugs. Although the long-acting somatostatin analog, octreotide, and the GnRH agonist, leuprolide, have shown prokinetic properties in particular clinical conditions, their widespread use cannot be recommended at present. Further work is needed to determine the predictive value of objective abnormalities for the efficacy of a drug in the individual patient. This is the crucial point to define a rational strategy in clinical practice, especially to establish if functional investigation is needed before a prokinetic drug be given.

show abstract

Somatostatin inhibits motilin-induced interdigestive contractile activity in the dog

Cited by 63 publications

References 18 publications

Amelioration of intestinal dysmotility and stasis by octreotide early after small-bowel autotransplantation in dogs

Amelioration of intestinal dysmotility and stasis by octreotide early after small-bowel autotransplantation in dogs

Somatostatin

Pharmacological Stimulation of Gastrointestinal Motility: Where We Are and Where Are We Going?

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