SUMMARY1. The effect of D-and L-isomers of tryptophan and phenylalanine on fasting motor activity of canine jejunum were investigated.2. Only L-tryptophan had any effect on jejunal motility. The concentration of L-tryptophan required to elicit a motor effect in 50 % of animals was estimated at 28 mM.3. 50 mM-L-tryptophan stimulated jejunal motility after a latency of 4-5 + 0-7 min. The pattern of motility was similar to that evoked by feeding but continued for only 41+5 min and failed to disrupt the normal timing of the interdigestive migrating motor complex (m.m.c.). The duration of the subsequent phase II of the complex was, however, significantly reduced.4. Multiple infusion of L-tryptophan also failed to disrupt the timing of the m.m.c. 5. These data are consistent with the hypothesis that specific breakdown components of protein digestion are implicated in the stimulation of postprandial motor activity. The mechanisms involved in the motor response to L-tryptophan are discussed.
SUMMARY1. The jejunal motor response to gastric distension has been quantified in the conscious dog and compared with that of feeding in order to determine the role of the physical bulk of a meal in the conversion from fasted to fed motor activity.2. In six dogs gastric distension abolished the cyclical migrating motor complex (m.m.c.) and evoked a pattern of continuous irregular jejunal motility similar to that seen postprandially, but only after a latency of 21 5±2'7 min compared to that of 7.1 + 1P2 min for the response to feeding. Computer analysis of distension and fed jejunal motility revealed similar distributions of intervals between contractions and contraction amplitudes with comparable mean values for both.3. In two dogs with antrum and corpus surgically divided distension of the corpus had a similar effect on jejunal motility although the latency to both distension and feeding were considerably less.4. By varying the period of distension it has been possible to control accurately the duration of the jejunal motor response and so assess its effectiveness in disrupting the timing of the m.m.c. The return to m.m.c. cycling following deflation was independent of preceding complexes. The occurrence of the post-distension activity front was closely related to the act of deflation itself (R = 094) following a latency of 26-2+21 min (n = 39).5. It is concluded that the bulk of a meal contributes significantly to the early part of postprandial motility and is capable of disrupting the timing of subsequent migrating motor complexes.
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