Gastrointestinal myoelectric activity was recorded in seven studies in five dogs during two hours of fasting immediately followed by feeding and subsequent recording for four hours. In four studies serial plasma samples were taken for radioimmunoassay of insulin and gastrin. In all animals there was a significant reduction (P less than 0.01) in gastric basic electrical rhythm (BER) frequency on feeding which was sustained throughout the postprandial period. There was no change in the duodenal BER. Feeding induced a significant (P less than 0.01) increase in overall jejunal and ileal (but not duodenal) spike activity. Ileal (but not jejunal) spike activity again increased significantly (P less than 0.05) after the first two post-prandial hours. The changes in serum gastrin or in serum insulin did not appear to account for most of the observed changes in myoelectric activity, suggesting that other humoral and/or neural factors mediate the response to food.

The effect of two-hour infusions of metoclopramide at five different doses on interdigestive intestinal electrical activity was studied in four conscious fasting dogs. Spike activity during the infusions was quantitatively compared with activity during preceding and following periods of saline infusion. The effect of the drug was the enhancement of spike activity during migrating myoelectric complexes (MMC) without disruption of the fasting pattern; the effect was most marked in the proximal small intestinal and diminished distally. As in other published studies with metoclopramide, its effects were variable and not dose dependent. The enhancement of the MMC by an exogenous stimulus, not previously reported, provides indirect evidence for cholinergic mediation of cyclical motor activity, and also suggests a rational basis for therapy.