Morphine Initiated Migrating Myoelectric Complexes in Post-Prandial State in Dog: Changes in Refractoriness of MMC Mechanism

Abstract

The ingestion of a meal in nonruminants disrupts the cycling of MMC’s for several hours. We investigated the initiation of phase III’s during the post-prandial state by morphine to elucidate the mechanism of disruption of MMC’s by a meal. Small intestinal recordings were made from 5 dogs by surgically implanted electrodes. Morphine boluses (5–400 pg/kg) were given during the fasted state and after a meal. Morphine initiated premature phase III’s in the fasted state and it also initiated phase III’s in the postprandial state. Motilin did not initiate phase III’s in the post-prandial state. The mean durations of morphine initiated phase III’s in the fasted state and in the postprandial state were not significantly different from that of spontaneous phase III’s. However, morphine initiated phase III’s in both the fasted and fed states propagated faster than spontaneous phase III’s in the proximal half of small intestine but not in the distal half. The latent period for the initiation of phase III’s was significantly greater 30–40 min after the meal than 2 hrs. after the meal. The minimum dose of morphine required to initiate a phase III 30–40 min after the meal was 3–4 fold higher than at a corresponding time in the fasted state. The minimum dose of morphine required to initiate a phase III decreased progressively after the initial increase till it reached fasted level 7–8 hrs after the meal. Spontaneous phase III’s appeared after this period. We conclude that (1) morphine overcomes the disruption of MMC cycling after a meal; (2) morphine acts at different sites than motilin to initiate phase III’s in the fed state; (3) the increased refractoriness of MMC mechanisms after a meal may play a role in the disruption of MMC cycling.