TY - JOUR
T1 - Role of Extrinsic Innervation in Release of Motilin and Patterns of Upper Gut Canine Motility
AU - Siadati, Mohammad
AU - Sar, Michael G.
N1 - Funding Information:
The need for extrinsic neural input to the upper gut in regulation/control of cyclic interdigestive motility and release of motilin remains a topic of controversy. Our aim was to determine whether extrinsic denervation of the upper gut disrupts cyclic release of motilin in relation to the migrating motor complex. Ten dogs underwent transection of all extrinsic innervation and enteric neural input to the stomach, small intestine, colon, pancreas, and liver while enteric neural continuity within this multivisceral complex was maintained. A cyclic pattern of motility occurred during fasting in all dogs in the small bowel (period = 100 -+ 3 min, mean -+ standard error of the mean) and in 8 of 10 dogs in the stomach (period = 98 -+ 4 min). Gastric cycles were temporally coordinated with small bowel cycles. Plasma motilin concentrations cycled temporally with the motility pattern with the greatest concentrations occurring during gastroduodenal phase m-like activity. Exogenous motilin induced a burst of gastric contractions and a premature migrating motor complex in all dogs. Oral meals disrupted cyclic motility and cyclic changes in plasma motilin. Extrinsic innervation to the upper gut is not necessary for cyclic motor activity, for coordinated cyclic release of motilin, or to initiate a premature migrating motor complex-like response to motilin. Central nervous system input (afferent, efferent) is not necessary for cyclic interdigestive activity or cyclic release of motilin. (J GASTROINTESTS URG 1998;2:363-372.) During the interdigestive (fasting) period, the upper gut of humans and most nonruminant mammals undergoes a characteristic cyclic pattern of motor activity termed the migrating motor complex (MMC).I,Z The MMC consists of four phases, 3 the most characteristic of which is phase III or the activity front, which is a burst of high-amplitude propulsive contractions. This band of contractile activity begins in the lower esophageal sphincter and stomach, then appears in the duodenum, and migrates down the length of the small intestine in a sequential orderly fashion propelling intraluminal debris and nondigestible content distally. As the phase III reaches the distal ileum, another phase III of the next cycle begins in the lower esophageal sphincter and stomach; this cycle repeats monotonously during fasting. Feeding disrupts the MMC and induces a noncyclic postprandial "fed" pattern of intermittent contractions that persist for a variable duration that is dependent on the characteristics and caloric content of the meal. 4 The mechanisms controlling these global motor patterns remain incompletely understood. Although migration of the MMC along the gut is controlled by continuity of the enteric nervous system, s the factor(s) that initiate the onset of phase IH activity in the stomach and duodenum is (are) not fully understood. Considerable experimental evidence supports both neural and hormonal modulatory roles in both the initiation and inhibition of these motor patterns. 1,6,7 Our previous work after complete neural isolation of the jejunoileum s,9 and after neural isolation of the stomach alone 1° showed the persistence of a cyclic motility pattern during fasting that was disrupted by oral meals. Similarly, previous observations in a model of in situ neural isolation of the upper gut suggested preservation of a cyclic motor pattern. 11 Because the From the Department of Surgerya nd GastroenterologyR esearchU nit, Mayo Clinic and Mayo Foundation, Rochester,M inn. Supported in part by United States Public Health Service grant DK39337 from the National Institutes of Health (M.G.S.) and by the Mayo Foundation. Presented in part at the President's Plenary Poster Session of the AmericanG astroenterologicalA ssociation, San Francisco, Calif., May 20-22, 1996, and published as an abstract in Gastroenterology 110:A758, 1996. Correspondence: Michael G. Sarr, M.D., Professor of Surgery, GastroenterologyR esearch Unit, Mayo Clinic, 200 First Street SW, Rochester, MN 55905.
PY - 1998
Y1 - 1998
N2 - The need for extrinsic neural input to the upper gut in regulation/control of cyclic interdigestive motility and release of motilin remains a topic of controversy. Our aim was to determine whether extrinsic denervation of the upper gut disrupts cyclic release of motilin in relation to the migrating motor complex. Ten dogs underwent transection of all extrinsic innervation and enteric neural input to the stomach, small intestine, colon, pancreas, and liver while enteric neural continuity within this multivisceral complex was maintained. A cyclic pattern of motility occurred during fasting in all dogs in the small bowel (period = 100 ± 3 min, mean ± standard error of the mean) and in 8 of 10 dogs in the stomach (period = 98 ± 4 min). Gastric cycles were temporally coordinated with small bowel cycles. Plasma motilin concentrations cycled temporally with the motility pattern with the greatest concentrations occurring during gastroduodenal phase III-like activity. Exogenous motilin induced a burst of gastric contractions and a premature migrating motor complex in all dogs. Oral meals disrupted cyclic motility and cyclic changes in plasma motilin. Extrinsic innervation to the upper gut is not necessary for cyclic motor activity, for coordinated cyclic release of motilin, or to initiate a premature migrating motor complex-like response to motilin. Central nervous system input (afferent, efferent) is not necessary for cyclic interdigestive activity or cyclic release of motilin.
AB - The need for extrinsic neural input to the upper gut in regulation/control of cyclic interdigestive motility and release of motilin remains a topic of controversy. Our aim was to determine whether extrinsic denervation of the upper gut disrupts cyclic release of motilin in relation to the migrating motor complex. Ten dogs underwent transection of all extrinsic innervation and enteric neural input to the stomach, small intestine, colon, pancreas, and liver while enteric neural continuity within this multivisceral complex was maintained. A cyclic pattern of motility occurred during fasting in all dogs in the small bowel (period = 100 ± 3 min, mean ± standard error of the mean) and in 8 of 10 dogs in the stomach (period = 98 ± 4 min). Gastric cycles were temporally coordinated with small bowel cycles. Plasma motilin concentrations cycled temporally with the motility pattern with the greatest concentrations occurring during gastroduodenal phase III-like activity. Exogenous motilin induced a burst of gastric contractions and a premature migrating motor complex in all dogs. Oral meals disrupted cyclic motility and cyclic changes in plasma motilin. Extrinsic innervation to the upper gut is not necessary for cyclic motor activity, for coordinated cyclic release of motilin, or to initiate a premature migrating motor complex-like response to motilin. Central nervous system input (afferent, efferent) is not necessary for cyclic interdigestive activity or cyclic release of motilin.
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U2 - 10.1016/S1091-255X(98)80076-0
DO - 10.1016/S1091-255X(98)80076-0
M3 - Article
C2 - 9841994
AN - SCOPUS:0032107784
SN - 1091-255X
VL - 2
SP - 363
EP - 372
JO - Journal of Gastrointestinal Surgery
JF - Journal of Gastrointestinal Surgery
IS - 4
ER -