Biliary sphincter motility after neural isolation of the pancreatoduodenal region in conscious dogs

Ohtsuka, Takao; Yokohata, Kazunori; Inoue, Ken; Nabae, Toshinaga; Takahata, Shunichi; Tanabe, Yoshitaka; Sugitani, Atsushi; Tanaka, Masao

doi:10.1067/msy.2002.118953

Cited by 11 publications

(9 citation statements)

References 29 publications

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“…In most mammals (including humans), the upper gastrointestinal tract exhibits as cyclic change in motor activity, called the migrating motor complex (MMC), during fasting. The MMC is divided into four phases (I–IV), with phase III being the most characteristic activity of the MMC, during which the upper gastrointestinal tract shows strong regular contractions of maximal frequency and amplitude ,. Gastric phase III activity occurs in the proximal stomach and migrates down to the duodenum, jejunum, and ileum, in that order.…”

Section: Motor Function Of the Gastrointestinal Tract After Pppdmentioning

confidence: 99%

“…The gastrointestinal MMC disappears immediately after feeding, and postprandial motor activity, consisting of irregular contractions of intermediate amplitude, similar to phase II of the MMC, continues for several hours. The occurrence of gastroduodenal phase III is associated with peak levels of plasma motilin concentrations ,. The main action of the phase III activity during fasting is to clean up the meal residue, basal secretions, and cellular debris from the gastrointestinal tract, and this activity is thus called “housekeeper” activity; the gastric phase III activity is also considered to be responsible for gastric emptying during the immediate postoperative period before the resumption of food intake.…”

Section: Motor Function Of the Gastrointestinal Tract After Pppdmentioning

confidence: 99%

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Gastrointestinal function and quality of life after pylorus-preserving pancreatoduodenectomy

Ohtsuka

Tanaka

Miyazaki

2006

J Hepatobiliary Pancreat Surg

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The pylorus-preserving pancreatoduodenectomy (PPPD) has taken the place of the conventional Whipple pancreatoduodenectomy as the standard procedure for various periampullary disease. With recent advances in surgical techniques and improvements in perioperative management, the number of long-term survivors after PPPD is increasing. As a result, surgeons should pay more attention to the patients' postoperative gastrointestinal function, nutrition, and quality of life (QOL). Gastric stasis, which is a frequent complication during the early postoperative period after PPPD, prolongs the hospital stay and impairs the QOL in the intermediate term. Several possible pathogeneses for this gastric stasis have been postulated; however, the precise mechanism remains unclear. The gastric emptying function gradually recovers to the preoperative level by 6 months after PPPD. Pancreatic functions are likely to be maintained for at least 1 year after PPPD; however, in some cases, they tend to gradually deteriorate over time after the operation, depending on the type of pancreatic reconstruction or the preoperative condition of the pancreas. It is important to note that preoperative and postoperative pancreatic exocrine function strongly influence the postoperative outcome regarding such factors as pancreatic fistula, body weight maintenance, nutrition, and the QOL. The QOL, as assessed by questionnaire, normally returns to the preoperative level within 6 months after PPPD, and this correlates with the changes in gastrointestinal function and nutritional status. It still remains an unresolved question, however, whether the Billroth-I PPPD really leads to better long-term nutritional status, but worse early gastric emptying function, than the Billroth-II type of reconstruction.

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Section: Motor Function Of the Gastrointestinal Tract After Pppdmentioning

confidence: 99%

Section: Motor Function Of the Gastrointestinal Tract After Pppdmentioning

confidence: 99%

Gastrointestinal function and quality of life after pylorus-preserving pancreatoduodenectomy

Ohtsuka

Tanaka

Miyazaki

2006

J Hepatobiliary Pancreat Surg

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“…The slow waves determine the contraction frequency in the GI tract. Receptors for a number of neurotransmitters have been located on ICC in the gut, including receptors for acetylcholine (M 2 , M 3 ), tachykinins (NK 1 , NK 3 ), vasoactive intestinal polypeptide (VPAC 1 ), adenosine triphosphate (ATP) (P2X 2 , P2X 5 ), and furthermore NO is also active on ICC 22–31 . Therefore ICC may play a pivotal, but currently under‐appreciated, role in controlling and/or modulating SO motility, and as such they should be considered in future functional studies.…”

Section: Control Of Spontaneous So Activitymentioning

confidence: 99%

The sphincter of Oddi: understanding its control and function

Woods

Mawe

Toouli

et al. 2005

Neurogastroenterology Motil

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The most common functional disorders of the biliary tract and pancreas are associated with disordered motility of the sphincter of Oddi (SO). The SO is a neuromuscular structure located at the junction of the bile and pancreatic ducts with the duodenum. The primary functions of the SO are to regulate the delivery of bile and pancreatic juice into the duodenum, and to prevent the reflux of duodenal contents into the biliary and pancreatic systems. Disordered motility of the SO leads to the common and painful clinical conditions of SO dysfunction and acute pancreatitis. In order to understand normal SO motility, studies have been performed addressing SO function, control of spontaneous SO activity, responses to bioactive agents, SO innervation, and reflexes with other gastrointestinal organs. These studies have led to the current understanding of how the SO functions and may permit the development of targeted therapy for SO dysfunction and acute pancreatitis. This review summarizes the current knowledge regarding the control and regulation of SO motility, highlighting laboratory based and clinical research performed over the last 5 years.

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“…When the whole duodenum was separated together with the intact SO, but with extrinsic denervation, new cyclic motor activities, with a higher frequency than that of the original MMC, were initiated in the duodenal segment. 12 In addition, the basal pressure and motility index of the SO were increased. In this model, CCK-8 evoked contractions of the SO, rather than evoking relaxation.…”

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confidence: 98%

Where is the primary site of action of CCK for initiating sphincter of Oddi relaxation?

Naruse

2005

J Gastroenterol

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The delivery of bile into the duodenum is controlled by the motor activity of the gallbladder and sphincter of Oddi (SO). 1 In humans and dogs, the SO acts as a resistor to the outflow of bile. During the interdigestive period, when there is no duodenal activity, the basal pressure and rhythmic contractions of the SO exceed the hepatic secretory pressure of bile, which results in the gradual filling of the gallbladder. Ingestion of a meal induces gallbladder contraction and relaxation of the SO via the release of cholecystokinin (CCK) and the vagal reflex. The gallbladder pressure is higher than the intraduodenal pressure, which allows entry of bile into the duodenum and prevents the regurgitation of the duodenal contents back into the biliary tract. In the fasting state, bile is cyclically secreted into the duodenum by periodic contractions of the gallbladder associated with the migrating motor complex (MMC) of the duodenum. 2 The gallbladder contraction occurs at the beginning of the phase-II contraction of the duodenum, 3 which is dependent on intact vagal innervation. 4 During phases II and III, when the duodenal pressure exceeds 100 mmHg, the contractions of the SO are coordinated in phase with those of the duodenum to prevent regurgitation. The SO and the duodenum act independently, but their functions are coordinated for the optimal duodenal delivery of bile. However, it is not known exactly how their coordination is controlled.Many physiological and anatomical studies 5 indicate the existence of neuronal connections between the duodenum and the biliary tract (the gallbladder and SO). The neurons of the SO are regulated by the parasympathetic (vagus) and sympathetic nerves, and by gut hormones, such as CCK. In addition, there is an intramural neural projection to the SO ganglia from the myenteric plexus of the duodenum in the Australian possum and guinea pig. 6,7 Physiological concentrations of CCK-around 5 pM following meal ingestion 8 -stimulate contractions of the gallbladder, where the smooth muscle cells express CCK-A (CCK1) receptors. 9 In humans and dogs, in which the SO acts as a resistor, CCK causes relaxation; it decreases the SO basal pressure and abolishes its phasic contractions. The relaxation appears to be mediated by neural mechanisms, as tetrodotoxin inhibits the relaxation evoked by CCK. 10 The candidates for inhibitory mediators are vasoactive intestinal peptide (VIP) and nitric oxide (NO). The stimulatory effect of CCK after the application of tetrodotoxin is probably a direct effect of CCK on the SO. Exogenous CCK elicits a paradoxical response (contraction) of the SO in some patients with biliary dyskinesia and in some patients who have undergone surgery of the upper gastrointestinal tract.In this issue of the Journal of Gastroenterology, Dong et al. 11 report their investigation of how surgical separation of the SO from the duodenum affected the SO response to CCK octapeptide (CCK-8). They found that an intravenous injection of CCK-8 failed to elicit SO inhibition in duodenectomized ...

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Biliary sphincter motility after neural isolation of the pancreatoduodenal region in conscious dogs

Cited by 11 publications

References 29 publications

Gastrointestinal function and quality of life after pylorus-preserving pancreatoduodenectomy

Gastrointestinal function and quality of life after pylorus-preserving pancreatoduodenectomy

The sphincter of Oddi: understanding its control and function

Where is the primary site of action of CCK for initiating sphincter of Oddi relaxation?

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