The possum sphincter of Oddi pumps or resists flow depending on common bile duct pressure: a multilumen manometry study

Grivell, Marlene B.; Woods, Charmaine M.; Grivell, Anthony R.; Neild, T O; Craig, Alexander; Toouli, James; Saccone, G. T. P.

doi:10.1113/jphysiol.2004.061663

Cited by 24 publications

(14 citation statements)

References 42 publications

(67 reference statements)

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“…It was found that the human sphincter of Oddi demonstrated unique phasic contractions, which would have an important role in regulating biliary and pancreatic duct emptying [65] . Several studies on the opossum sphincter of Oddi showed that it regulates bile like a peristaltic pump at low common bile duct pressure and as a resistor at higher common bile duct pressures [66][67][68] . Funch-Jensen et al [69] observed that the CCK injection inhibited the activity of the sphincter of Oddi of dogs, thus as bile flow increased, the gallbladder pressure remained unchanged.…”

Section: Geometry Of Biliary Duct and Flow Resistancementioning

confidence: 99%

On the mechanical behavior of the human biliary system

Luo

Li²,

Bird³

et al. 2007

WJG

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This paper reviews the progress made in understanding the mechanical behaviour of the biliary system. Gallstones and diseases of the biliary tract affect more than 10% of the adult population. The complications of gallstones, i.e. acute pancreatitis and obstructive jandice, can be lethal, and patients with acalculous gallbladder pain often pose diagnostic difficulties and undergo repeated ultrasound scans and oral cholecystograms. Moreover, surgery to remove the gallbladder in these patients, in an attempt to relieve the symptoms, gives variable results. Extensive research has been carried out to understand the physiological and pathological functions of the biliary system, but the mechanism of the pathogenesis of gallstones and pain production still remain poorly understood. It is believed that the mechanical factors play an essential role in the mechanisms of the gallstone formation and biliary diseases. However, despite the extensive literature in clinical studies, only limited work has been carried out to study the biliary system from the mechanical point of view. In this paper, we discuss the state of art knowledge of the fluid dynamics of bile flow in the biliary tract, the solid mechanics of the gallbladder and bile ducts, recent mathematical and numerical modelling of the system, and finally the future challenges in the area.

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Section: Geometry Of Biliary Duct and Flow Resistancementioning

confidence: 99%

On the mechanical behavior of the human biliary system

Luo

Li²,

Bird³

et al. 2007

WJG

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“…A custom-built five-lumen picomanometry catheter was positioned in the biliary component of the SO via a small incision in the common bile duct [6,20]. Each catheter lumen was connected to a pressure transducer (Sorenson Transpac disposable transducer; Abbot Critical Care Systems, USA) and perfused with saline (0.02 ml/min/lumen) via a low-compliance pneumohydraulic capillary infusion system (Dentsleeve Pty.…”

Section: Surgical Preparationmentioning

confidence: 99%

“…The manometry catheter was positioned within the SO to record proximal-SO, body-SO, and distal-SO activity ( Fig. 1B) [6]. All pressure transducers were connected to a MacLab recording system (MacLab/8S; ADInstruments, Castle Hill, Australia) and the software Chart v3.6/s (ADInstruments) was utilized.…”

Section: Surgical Preparationmentioning

confidence: 99%

Exogenous Adenosine Triphosphate and Adenosine Stimulate Proximal Sphincter of Oddi Motility Via Neural Mechanisms in the Anesthetized Australian Possum

2006

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We aimed to determine if exogenous adenosine triphosphate or adenosine modulated sphincter of Oddi motility and involved neural mechanisms. Sphincter of Oddi motility was recorded in anesthetized possums by manometry. Adenosine triphosphate or adenosine (1 microM-10 mM) was applied topically to the sphincter before and after pretreatment with tetrodotoxin, hexamethonium, atropine, or Nomega-nitro-L-arginine methyl ester. Sphincter contraction amplitude and frequency were quantified. Adenosine triphosphate induced a concentration-dependent increase in proximal sphincter contraction amplitude and frequency (P < 0.05). This response was reduced by tetrodotoxin and atropine but enhanced by hexamethonium and Nomega-nitro-L-arginine methyl ester. Adenosine concentration dependently increased proximal sphincter contraction amplitude (P < 0.05) only. This response was reduced by tetrodotoxin, atropine, and Nomega-nitro-L-arginine methyl ester, whereas hexamethonium had no effect. We conclude that exogenous adenosine triphosphate and adenosine stimulate proximal sphincter of Oddi motility via neural mechanisms, involving cholinergic motor neurons. Adenosine triphosphate may further modulate sphincter motility via nicotinic and nitrergic pathways.

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“…This organ is connected to the duodenum via extrinsic nerves, 5 and the SO function may be modified depending on common duct pressure. 17 There is significant redundancy in the regulatory mechanisms of the gastrointestinal tract. When one mechanism is severely disturbed, other mechanisms may take over the function of the primary one, to maintain the integrity.…”

mentioning

confidence: 99%

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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The possum sphincter of Oddi pumps or resists flow depending on common bile duct pressure: a multilumen manometry study

Cited by 24 publications

References 42 publications

On the mechanical behavior of the human biliary system

On the mechanical behavior of the human biliary system

Exogenous Adenosine Triphosphate and Adenosine Stimulate Proximal Sphincter of Oddi Motility Via Neural Mechanisms in the Anesthetized Australian Possum

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

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