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Gastrointestinal motility was studied in conscious sheep by X-radiography and by electromyography from chronically implanted electrodes before and after total thoracic vagotomy. Duodenal infusion of 0.5-3 mmol HCl (0.035-0.1 M-HCl) induced premature duodenal regular spiking activity (r.s.a.) within 1-7 min in fifteen of seventeen sheep studied when infused at 20 min after a natural r.s.a. There was no correlation between abomasal pH and any phase of the migrating myoelectric complex (m.m.c.). Duodenal alkalinization by infusion of 0.3 M-Tris buffer (pH 10.2) or 0.1 M-NaHCO3 had no influence on the occurrence of the m.m.c. Duodenal infusion of 20-50 ml 0.5 M-NaCl induced a premature duodenal r.s.a. within 1-5 min in seven of eight sheep. Vagotomy did not prevent the initiation or migration of the m.m.c., but reduced the rate of propagation of the r.s.a. from 40.5 +/- 7.2 (mean +/- S.E. of mean) to 16.7 +/- 0.1 cm/min in the duodenum, from 27.3 +/- 4.1 to 16.6 +/- 0.8 cm/min in the jejunum, and from 21.4 +/- 1.1 to 13.7 +/- 0.7 cm/min in the proximal ileum. Initially the frequency of r.s.a. increased, especially in the duodenum where they recurred at an interval of 98.4 +/- 6.8 min before vagotomy; and at 23.4 +/- 1.8 min in the first 24 h after vagotomy; the interval had lengthened to 86.7 +/- 5.2 min 2-3 weeks after vagotomy. Premature duodenal r.s.a. was not induced by duodenal infusion of HCl in five, or by duodenal infusion of hyperosmolar NaCl in three chronically vagotomized sheep. It is concluded that the vagus nerves contribute to the regulation of the frequency and propagation of the m.m.c. in sheep; duodenal acidification is not essential nor is it the normal stimulus for initiation of r.s.a., but duodenal infusion of HCl or hyperosmolar NaCl can initiate a premature duodenal r.s.a. via the vagus nerves.

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