Small intestinal amyogenesia and dysmyogenesia induced by morphine and loperamide

We studied the effects of morphine and loperamide on small bowel myoelectric and contractile activity in 12 conscious dogs. After initially producing premature migrating myoelectric complexes, both substances destabilized and obliterated electrical control activity (ECA). The obliteration of ECA occurred mainly in the proximal half of the small intestine. During ECA obliteration, the base line was almost flat at the usual amplification. At higher amplification, the base line exhibited irregular low level fluctuations that could not be related to electrical response activity (ERA) bursts or contractions. The mean time lag for obliteration of ECA in the proximal small intestine decreased at higher doses of morphine infusion. During the destabilization and obliteration of ECA, contractions and ERA bursts occurred in unusual patterns. The ERA bursts and contractions were generally discoordinated. However, in the proximal small intestine some contractions migrated rapidly and uninterrupted at 32 +/- 7 cm/s over long distances (124 +/- 24 cm). ECA destabilization and obliteration were reversed in approximately 15-30 min after the ingestion of a meal or intravenous administration of atropine, hexamethonium, or naloxone. We conclude that during the absence or destabilization of ECA, the ERA bursts and contractions occur in an uncontrolled manner. These two states were called "amyogenesia" and "dysmyogenesia," respectively. The unusual patterns of contractions during small intestinal amyogenesia and dysmyogenesia may be one of the factors in delayed intestinal transit produced by morphine and loperamide.