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Disruption of the jejunal migrating motor complex by gastric distension and feeding in the dog.
Author(s) -
Bull J S,
Grundy D,
Scratcherd T
Publication year - 1987
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1987.sp016876
Subject(s) - distension , postprandial , migrating motor complex , motility , gastric distension , antrum , meal , medicine , jejunum , vagotomy , endocrinology , motor activity , pyloric antrum , stomach , chemistry , biology , anatomy , insulin , genetics
1. 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 +/‐ 1.2 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 = 0.94) following a latency of 26.2 +/‐ 2.1 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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