Characteristics of secretin‐stimulated pancreatic secretion in dogs.

Maggee, D F; Naruse, Satoru

doi:10.1113/jphysiol.1984.sp015472

Cited by 11 publications

(6 citation statements)

References 9 publications

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“…Others have confirmed these findings. [5][6][7] Tanaka and Sarr 8 reported that duodenectomy disrupts not only the coordination of gastric and intestinal migrating motor complexes (MMC) but also the coordination between interdigestive motility and pancreatic secretion, and it abolishes the interdigestive cyclic variations in plasma motilin and pancreatic polypeptide (PP) levels. 9 The release of PP appears to be regulated by a complex interplay between neural input (from the vagus) and humoral factors that originate from the upper gut.…”

Section: Discussionmentioning

confidence: 99%

Effect of Duodenectomy on Gastric Motility and Gastric Hormones in Dogs

Suzuki¹,

Mochiki²,

Haga³

et al. 2001

Annals of Surgery

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ObjectiveTo test the hypothesis that the duodenum is required to coordinate interdigestive insulin secretion with gastrointestinal motility and to determine whether duodenectomy alters the interdigestive cycles of plasma motilin and insulin levels and their relations to insulin secretion and motility. MethodsAdult mongrel dogs were chronically implanted with force transducers in the stomach, duodenum, and upper jejunum to monitor contractile activity. Eight healthy mongrel dogs were divided into control and duodenectomized dogs. Insulin secretion, gastrointestinal motility, and plasma concentrations of motilin during the interdigestive period were measured in normal and duodenectomized dogs. ResultsAfter duodenectomy, no obvious phase III contractions were seen in the gastric antrum, but migrating phase III contractions were seen in the upper jejunum. The plasma motilin concentration did not fluctuate as it does in normal dogs, and remained low. After duodenectomy, insulin secretory cycles were not coordinated with either cycles of interdigestive motility or the plasma concentration of motilin. Exogenous motilin administration stimulated endogenous insulin release significantly compared with saline-treated controls. The contractile response of the stomach to exogenous motilin after duodenectomy was similar to that of intact dogs. ConclusionsDuodenectomy disrupts the relation between cycles of both interdigestive gastrointestinal motility and insulin secretion. These effects of duodenectomy may be attributable to interruption of the duodenopancreatic neural connections, hormonal abnormalities, or loss of vagus-sensitive humoral factors. The duodenum, which stores motilin, seems to play an important role in the relations between gastric migrating motor complexes and the concomitant increase of insulin secretion in fasted dogs. The mechanism responsible for the effect of motilin in both duodenectomized and normal dogs may involve a cholinergic pathway.The duodenum occupies a strategic anatomical position in the upper digestive tract and is intimately involved in the coordination of various functions of the upper gut. It influences gastric empting, 1 pancreatic and biliary secretion, 2 and the organization and initiation of gastric motor patterns 3,4 by invoking hormonal and neural mechanisms. Others have confirmed these findings.5-7 Tanaka and Sarr 8 reported that duodenectomy disrupts not only the coordination of gastric and intestinal migrating motor complexes (MMC) but also the coordination between interdigestive motility and pancreatic secretion, and it abolishes the interdigestive cyclic variations in plasma motilin and pancreatic polypeptide (PP) levels. 9 The release of PP appears to be regulated by a complex interplay between neural input (from the vagus) and humoral factors that originate from the upper gut. 10,11The duodenum also plays an important role by regulating the release of certain pancreatic hormones. For example, intraduodenal glucose administration causes the release of more insulin than does...

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Section: Discussionmentioning

confidence: 99%

Effect of Duodenectomy on Gastric Motility and Gastric Hormones in Dogs

Suzuki¹,

Mochiki²,

Haga³

et al. 2001

Annals of Surgery

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“…the period of quiescence with no spiking activity (NSA) in the duodenal migrating myoelectric complex (MMC), and secretion increased intermittently before or during phase III, the period of regular spiking activity (RSA), concomitant with plasmal elevations of motilin, gastrin and pancreatic polypeptide (PP). The periodic secretory patterns were interrupted for several hours by feeding ) and were influenced by exogenous secretin, pentagastrin and CCK-8 (Magee & Naruse, 1984, 1988Thor, Laskiewicz, Konturek & Konturek, 1988).…”

Section: Introductionmentioning

confidence: 99%

Periodic fluctuations in pancreatic secretion and duodenal motility investigated in neonatal calves

Zabielski¹,

Onaga²,

Hashiguchi³

et al. 1993

Experimental Physiology

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SUMMARYTo clarify the relative timing of clinical changes in duodenal motility and pancreatic secretion in newborn calves, we recorded duodenal electrical and mechanical activity and analysed pancreatic secretion and migrating myoelectric complex (MMC). In eight calves integrated recordings were derived from sites near the duodenal bulb and pancreatic accessory duct orifice, and pancreatic juice was sampled after an overnight fast, after a feed, and during reversible cold vagal blockade. Peak secretion coincided with duodenal irregular spiking activity and the nadir with absence of spiking. Feeding elicited electrical and mechanical hyperactivity in the duodenum, dissipated the MMC temporarily, and dramatically increased the juice volume and bicarbonate and protein outputs. Periodic fluctuations in secretion started shortly after a feed, as did recovery of the duodenal myoelectric complexes. Cold vagal blockade reversibly disrupted the synchronous changes in duodenal motility and pancreatic secretory activity, though the close association was not totally obliterated. In milk-fed calves interdigestive pancreatic secretion apparently rises and falls in phase with migrating myoelectric complexes of the proximal duodenum and the vagus is largely, though not exclusively, responsible for co-ordinating these changes.

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“…The present study has shown that in the fasting dog as much as 50% of the observed maximal protein response to CCK-8 is spontaneously secreted from the pancreas, though the peak volume is less than 10 % of the maximum (Magee & Naruse, 1984). The average protein secretion in one cycle was about 17 % of the maximum.…”

Section: Discussionmentioning

confidence: 83%

“…The periodicity of basal secretion and neural activity of the pancreas, associated with gastroduodenal motility, has been unrecognized or ignored until recently (Magee & Naruse, 1983). Fluid and bicarbonate responses to physiological doses of secretin are potentiated by spontaneous periodic neural activities (Magee & Naruse, 1984). The peak pancreatic bicarbonate response to a fixed dose of secretin can be 18-7 times as much as the nadir response and the potentiation is completely blocked by atropine or ganglionic blockade.…”

Section: Introductionmentioning

confidence: 99%

The effect of cholecystokinin‐related peptides on periodic pancreatic secretion in fasting dogs.

Magee

Naruse

1988

The Journal of Physiology

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1. The effect of cholecystokinin octapeptide (CCK‐8) and pentagastrin on periodic pancreatic secretion was studied in fasting conscious dogs. 2. Both CCK‐8 and pentagastrin, in small doses, prolonged the interval of periodic pancreatic secretion. Periodicity was disrupted by large doses of CCK‐8 and pentagastrin. 3. CCK‐8, at the dose which did not disrupt the cycle, raised the peak and the valley‐to‐valley means, but not the valley mean, of protein secretion in one cycle. Except at large doses, pentagastrin failed to increase the peak and valley mean, but increased mean, valley‐to‐valley protein secretion. Large doses of both pentagastrin and CCK‐8 increased protein secretion at the valley. 4. The peak of periodic pancreatic protein secretion was about half the observed maximum protein response to CCK‐8. 5. Atropine reduced pancreatic fluid and protein responses to small doses of CCK‐8 to the levels of valleys. At large doses, however, both responses were augmented by atropine. Hexamethonium reduced the responses to any dose of CCK‐8 to valley levels or less. Volume and protein responses to pentagastrin following atropine or hexamethonium were of similar magnitude to those at valleys. 6. It is concluded that CCK‐8 and pentagastrin stimulate pancreatic enzyme secretion directly by acting on acinar cells and indirectly by modifying cholinergic ganglionic activities which control periodic secretion in conscious dogs.

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Characteristics of secretin‐stimulated pancreatic secretion in dogs.

Cited by 11 publications

References 9 publications

Effect of Duodenectomy on Gastric Motility and Gastric Hormones in Dogs

Effect of Duodenectomy on Gastric Motility and Gastric Hormones in Dogs

Periodic fluctuations in pancreatic secretion and duodenal motility investigated in neonatal calves

The effect of cholecystokinin‐related peptides on periodic pancreatic secretion in fasting dogs.

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