Cause-and-effect relationships between motilin and migrating myoelectric complexes

S. Sarna, W. Y. Chey, R. E. Condon

Research output: Contribution to journalArticle

Abstract

We investigated the cause-and-effect relationship betweeb plasma motilin levels and migrating myoelectric complexes (MMCs). Each dog was implanted with set of eight bipolar electrodes on the small intestine. Premature phase IIIs were initiated by morphine bolus injections. Plasma samples were assayed for motilin and gastrin. All spontaneous and morphine-initiated phase IIIs were associated with peaks of plasma motilin, which always occurred after phase IIIs had started in the proximal duodenum. The plasma motilin level decreased consistently during phase I and started to increase again only after phase II had started in the duodenum. Either a meal or somatostatin infusion disrupted MMC cycling, but morphine boluses overcame this disruption and initiated phase IIIs that propagated distally. The phase IIIs thus initiated were associated with peaks in plasma motilin levels. In contrast, bolus injections of motilin did not initiate phase IIIs during the fed state of during somatostatin infusion. Our findings suggest that endogenous motilin does not initiate spontaneous MMCs. Instead, MMC contractions release motilin. The physiological rule of motilin, thus released, may be to act as an endocrine agent to coordinate secretory and motor events with the start of phase III activity in the upper small intestine.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume8
Issue number2
StatePublished - 1983
Externally publishedYes

Fingerprint

Migrating Myoelectric Complexes
Motilin
Morphine
Somatostatin
Duodenum
Small Intestine
Injections
Gastrins
Meals
Electrodes
Dogs

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology

Cite this

Cause-and-effect relationships between motilin and migrating myoelectric complexes. / Sarna, S.; Chey, W. Y.; Condon, R. E.

In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 8, No. 2, 1983.

Research output: Contribution to journalArticle

@article{38f2c0bbac8e442eb0d8e1298517726b,
title = "Cause-and-effect relationships between motilin and migrating myoelectric complexes",
abstract = "We investigated the cause-and-effect relationship betweeb plasma motilin levels and migrating myoelectric complexes (MMCs). Each dog was implanted with set of eight bipolar electrodes on the small intestine. Premature phase IIIs were initiated by morphine bolus injections. Plasma samples were assayed for motilin and gastrin. All spontaneous and morphine-initiated phase IIIs were associated with peaks of plasma motilin, which always occurred after phase IIIs had started in the proximal duodenum. The plasma motilin level decreased consistently during phase I and started to increase again only after phase II had started in the duodenum. Either a meal or somatostatin infusion disrupted MMC cycling, but morphine boluses overcame this disruption and initiated phase IIIs that propagated distally. The phase IIIs thus initiated were associated with peaks in plasma motilin levels. In contrast, bolus injections of motilin did not initiate phase IIIs during the fed state of during somatostatin infusion. Our findings suggest that endogenous motilin does not initiate spontaneous MMCs. Instead, MMC contractions release motilin. The physiological rule of motilin, thus released, may be to act as an endocrine agent to coordinate secretory and motor events with the start of phase III activity in the upper small intestine.",
author = "S. Sarna and Chey, {W. Y.} and Condon, {R. E.}",
year = "1983",
language = "English (US)",
volume = "8",
journal = "American Journal of Physiology - Endocrinology and Metabolism",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "2",

}

TY - JOUR

T1 - Cause-and-effect relationships between motilin and migrating myoelectric complexes

AU - Sarna, S.

AU - Chey, W. Y.

AU - Condon, R. E.

PY - 1983

Y1 - 1983

N2 - We investigated the cause-and-effect relationship betweeb plasma motilin levels and migrating myoelectric complexes (MMCs). Each dog was implanted with set of eight bipolar electrodes on the small intestine. Premature phase IIIs were initiated by morphine bolus injections. Plasma samples were assayed for motilin and gastrin. All spontaneous and morphine-initiated phase IIIs were associated with peaks of plasma motilin, which always occurred after phase IIIs had started in the proximal duodenum. The plasma motilin level decreased consistently during phase I and started to increase again only after phase II had started in the duodenum. Either a meal or somatostatin infusion disrupted MMC cycling, but morphine boluses overcame this disruption and initiated phase IIIs that propagated distally. The phase IIIs thus initiated were associated with peaks in plasma motilin levels. In contrast, bolus injections of motilin did not initiate phase IIIs during the fed state of during somatostatin infusion. Our findings suggest that endogenous motilin does not initiate spontaneous MMCs. Instead, MMC contractions release motilin. The physiological rule of motilin, thus released, may be to act as an endocrine agent to coordinate secretory and motor events with the start of phase III activity in the upper small intestine.

AB - We investigated the cause-and-effect relationship betweeb plasma motilin levels and migrating myoelectric complexes (MMCs). Each dog was implanted with set of eight bipolar electrodes on the small intestine. Premature phase IIIs were initiated by morphine bolus injections. Plasma samples were assayed for motilin and gastrin. All spontaneous and morphine-initiated phase IIIs were associated with peaks of plasma motilin, which always occurred after phase IIIs had started in the proximal duodenum. The plasma motilin level decreased consistently during phase I and started to increase again only after phase II had started in the duodenum. Either a meal or somatostatin infusion disrupted MMC cycling, but morphine boluses overcame this disruption and initiated phase IIIs that propagated distally. The phase IIIs thus initiated were associated with peaks in plasma motilin levels. In contrast, bolus injections of motilin did not initiate phase IIIs during the fed state of during somatostatin infusion. Our findings suggest that endogenous motilin does not initiate spontaneous MMCs. Instead, MMC contractions release motilin. The physiological rule of motilin, thus released, may be to act as an endocrine agent to coordinate secretory and motor events with the start of phase III activity in the upper small intestine.

UR - http://www.scopus.com/inward/record.url?scp=0020599420&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020599420&partnerID=8YFLogxK

M3 - Article

VL - 8

JO - American Journal of Physiology - Endocrinology and Metabolism

JF - American Journal of Physiology - Endocrinology and Metabolism

SN - 0193-1849

IS - 2

ER -