Selective role of vagal and nonvagal innervation in initiation and coordination of gastric and small bowel patterns of interdigestive and postprandial motility.
Our previous studies suggested that extrinsic innervation modulates upper gut motility but is not requisite for cyclic interdigestive and postprandial motility of the stomach. However, the specific role of vagal and nonvagal extrinsic innervation in the initiation, coordination, and pattern of gastric motility in dogs after denervation of the entire upper gastrointestinal tract remains unclear. The aim of this study was to determine the role of vagal and nonvagal extrinsic innervation in control of gastric motility patterns. Mongrel dogs were subjected first to extrinsic denervation (in situ neural isolation) of the stomach, small bowel, proximal colon, liver, and pancreas but specifically maintaining vagal innervation to the stomach alone. After fasting and fed motility patterns were measured with indwelling gastric and small bowel manometry catheters, the dogs underwent transthoracic truncal vagotomy (completion of total extrinsic denervation of stomach), and motility studies were repeated. Vagal integrity to the stomach and pancreas was confirmed by means of a modified Hollander test and serum pancreatic polypeptide concentrations after the injection of exogenous insulin, respectively. We found that a cyclic motility pattern (migrating motor complex) persisted during fasting in both the stomach and the small bowel and that the patterns of the stomach and the duodenum remained temporally coordinated before and after vagotomy. However, although a cyclic phase III activity persisted in the stomach after vagotomy, the number of contractions and the motility index during phase III were decreased, and the duration between groupings of contractions was increased. No differences were noted in the duration of postprandial inhibition after feeding meals before and after vagotomy. These observations support our hypothesis that the vagal nerves are not necessary for the initiation or temporal coordination of global fasting or postprandial gastroduodenal motility patterns but are involved in modulating the pattern of contractions during gastric phase III.
Tanaka
T
T
Gastroenterology Research Unit, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, U.S.A.
VanKlompenberg
L H
LH
Sarr
M G
MG
D000818:Animals; D004285:Dogs; D005260:Female; D005745:Gastric Acidity Determination; D005769:Gastrointestinal Motility / Q000187:drug effects / Q000502:physiology*; D007328:Insulin / Q000494:pharmacology; D008365:Manometry; D009037:Motilin / Q000494:pharmacology; D016065:Myoelectric Complex, Migrating / Q000502:physiology; D010191:Pancreatic Polypeptide / Q000097:blood; D019518:Postprandial Period / Q000502:physiology*; D013997:Time Factors; D015167:Vagotomy, Truncal; D014630:Vagus Nerve / Q000502:physiology*
D007328:Insulin; D009037:Motilin; D010191:Pancreatic Polypeptide