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

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Abstract
The cause-and-effect relationshp between plasma motilin levels and migrating myoelectric complexes (MMC) was investigated. Each dog was implanted with a set of 8 bipolar electrodes on the small intestine. Premature phase III were initiated by morphine bolus injections. Plasma samples were assayed for motilin and gastrin. All spontaneous and morphine-initiated phase III were associated with peaks of plasma motilin, which always occurred after phase III 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 III that propagated distally. The phase III thus initiated were associated with peaks in plasma motilin levels. In contrast, bolus injections of motilin did not initiate phase III during the fed state or during somatostatin infusion. Endogenous motilin apparently does not initiate spontaneous MMC. Instead, MMC contractions release motilin. The physiological role 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.