[Analytical study on the extrahepatic biliary system by cholescintigraphy. I. An investigation on the motor dysfunction of the biliary system (author's transl)].
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Ampulla of Vater↗
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Results for “Sphincter of Oddi Dysfunction”
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The role of sphincter of Oddi manometry in the diagnosis and therapy of pancreatic disease.
Endoscopic manometry of the sphincter of Oddi (SO) is now an accepted technique in the diagnosis and therapy of biliary disease. Its role in the evaluation of pancreatic sphincter function for pancreatic diseases, however, is evolving. There are now preliminary data to suggest that pancreatic SO manometry may identify a subgroup of patients with pancreatic sphincter dysfunction that may benefit from endoscopic therapy. Further prospective clinical trials are sorely needed to evaluate the response of endoscopic therapy based on pancreatic SO basal pressure or pancreatic ductal pressure.
Cholangiopancreatography, Endoscopic Retrograde↗
The sphincter of Oddi: understanding its control and function.
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.
Animals↗
The effects of cholecystojejunostomy and biliary drainage on biliary motor.
Simulating physiological neuronal and hormonal conditions during digestive and interdigestive periods, the study identified the changes of the motility of biliary system including bile duct and sphincter of Oddi (SO) before and after cholecystojejunostomy. Thirty-five rabbits were divided into five groups randomly. The experimental groups received the venous injection of CCK 10 ng/kg, erythromycin 10 mg/kg, atropine 3 micrograms/kg and L-NAME 10 mg/kg respectively. Each rabbit underwent manometry through introducing a three-lumen catheter via the papilla retrogradely, using the low-compliance papillary infusion system. Then the gallbladder and the upper segment of the jejunum was anastomosed and the manometric procedures repeated after one week. SO basal pressure was increased, contraction amplitude decreased, contraction time shortened after cholecystojejunostomy. L-NAME, CCK and erythromycin could all excite SO. L-NAME could increase basal pressure and contraction amplitude, CCK increase basal pressure contraction amplitude and frequency, and erythromycin increase contraction amplitude, respectively. But comparing with that before cholecystojejunostomy, the increasing extent was decreased. The tensional and spontaneous contractions of the SO were under the control of the neural and hormonal mechanism. The anastomosis of gallbladder and jejunum and the drainage of bile made the tensional contraction stronger, but the spontaneous contraction weakened after the operation due to the decreases of the sensitivity of SO to hormonal factors. The clinical symptoms may not be relieved when the patients with SO dysfunction accepted cholecystojejunostomy.
Animals↗
[Vesicosphincter dysfunction in chronic liver diseases].
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Ampulla of Vater↗
The role of the flow rate of the pneumohydraulic system on post-sphincter of Oddi manometry pancreatitis.
Manometry of sphincter of Oddi (SO) carries a risk of acute pancreatitis by a mechanism not yet clearly understood. This study attempted to evaluate the role of the flow rate of the perfusion system in the development of acute pancreatitis. During the past 60 months, we have performed 81 manometry studies of SO in 79 patients, 61 women and 18 men, who were referred for recurrent attacks of abdominal pain suggestive of SO dysfunction. All procedures were done by the same operator, utilizing the same instrumentation and similar premedication. In the first 54 studies, the pneumohydraulic system had a flow rate of 0.55 ml/min and a tank pressure of 15 lb/in2 while in the last 27 studies a flow rate of 0.27 ml/min and a pressure of 7.5 lb/in2 were employed. Acute pancreatitis was diagnosed after 16 (19.7%) procedures. Fourteen (26%) of them occurred after high-flow-rate perfusion. In contrast, only 2 (7%) of the 27 patients who had the procedure done at the flow rate developed this complication (p less than 0.05). There was no correlation between the occurrence of pancreatitis, clinical suspicion of SO dysfunction, and the underlying manometric profile of the sphincter. We conclude that the incidence of procedure-related pancreatitis after manometry of SO is higher than following diagnostic endoscopic retrograde cholangiopancreatography and that the flow rate in the perfusion system is a precipitating factor in the development of this complication.
Acute Disease↗
[Dynamics of biliary prostaglandin secretion in patients with dyskinesia of the biliary tracts].
The time course of biliary secretion of prostaglandins (PG)E1 and F2 alpha was studied in 20 patients with primary dysfunctions in the cholepoietic system. The studies indicated that baseline high PGE1 levels and slow increases in PGF2 alpha during vesical reflex might be one of the factors predisposing to biliary hypokinesia. In patients with Oddi's sphincter spasms, the period of active PGE1 synthesis coincides with that of sphincter spasm. It is suggest that the latter is due to PGE1-induced muscle spasm of the duodenum whose fibers are an integral part of the intricate muscle system of Oddi's sphincter. In Oddi's sphincter spasm concurrent with biliary dyskinesia, the curve of PGF2 alpha virtually little differs from that in Oddi's sphincter spasm alone. PGE1 increases at the closed sphincter stage in the same way as that elevates in isolated sphincter spasm, but in patients with biliary hypokinesia contaminant with Oddi's sphincter spasm PGE1 shows its concentration in the vesical reflex phase, which appears to result in biliary hypokinesia. PGE1 and PGF2 alpha imbalance is one of the links in the pathogenesis of biliary dyskinesia.
Adult↗
Studies on papillary function and effect of prifinium bromide and other antispasmodics on motility of the papillary region (sphincter of Oddi) in humans.
We determined endoscopically the motility of the papillary region in humans, using a pressure sensor devised in our department. The subjects were 184 patients with various diseases. Prifinium bromide and four other antispasmodics were given to 60 of the 184 patients, and their effects were investigated. In 41 (85%) of the 48 patients with chronic gastritis, regular wave patterns were noted. In 35 (85%) of the 41 patients with diseases of the biliary tract and papillary region, in nine (82%) of the 11 patients with pancreatic diseases, and in six (67%) of the nine patients with liver diseases, irregular wave patterns were observed. It was postulated that a high incidence of papillary dysfunction accompanies biliary and pancreatic diseases. Additionally, it was concluded that prifinium bromide has as potent an effect on motility of the papillary region as does a massive dose (40 mg) of hyoscine N-butylbromide.
Adult↗
[Propofol sedation in endoscopic manometry of Oddi's sphincter].
Endoscopic manometry of the sphincter Oddi (SO) is a sophisticated method which requires a cooperative patient. Therefore, during endoscopic manometry sufficient i.v. sedation is crucial, and additionally must no affect SO-motility. In a pilot trial SO-motility was determined in ten patients with suspected SO-dysfunction (SOD) under initial sedation with 4.8 +/- 1 mg midazolam (baseline), and 3 min after an i.v. bolus of 50 mg of propofol. In addition, endoscopic manometry was performed in 57 consecutive patients with suspected SOD from 10/94-9/95 under sedation with midazolam (6.2 +/- 1.6 mg), and from 10/95-9/96 with propofol (268 +/- 111 mg). Sedation was always performed by an independent physician according to a standardized protocol. Neither the SO-baseline pressure nor the parameters of phasic SO-motility were significantly altered by propofol (including two patients with proven SOD). Propofol causes a more rapid onset of sedation, and the time interval to obtain successful biliary cannulation was shorter than under midazolam (p < 0.05). Successful manometric recordings could be obtained in 82% of the patients under midazolam but in 96% of the patients under propofol-sedation (p < 0.05), respectively. The patient cooperation was significantly better rated (by the endoscopist) in the propofol group than in the midazolam group (p < 0.01). The blood pressure and the heart rate were not significantly affected in both groups, however, propofol caused a significant decrease of the oxygen saturation (p < 0.05). Accordingly, an apnea episode had to be mastered by mask ventilation via ambu bag in one patient under propofol-sedation (uneventful recovery). In the midazolam group flumazenil-administration was necessary in four patients. The post-procedure recovery was faster after propofol--than after midazolam-sedation (p < 0.05). In conclusion, propofol is suitable for i.v. sedation during endoscopic manometry of the spincter of Oddi.
Adult↗
ERCP, biliary crystal analysis, and sphincter of Oddi manometry in idiopathic recurrent pancreatitis.
BACKGROUND: This study investigated the role of ERCP, analysis of bile for microcrystals, and sphincter of Oddi manometry in idiopathic recurrent pancreatitis. METHODS: One hundred twenty-six patients met criteria for idiopathic recurrent pancreatitis. Patients with a normal ERCP underwent sphincter of Oddi manometry and analysis of bile. Bile was also collected in patients with papillary stenosis (defined as ductal dilation with delayed drainage of contrast, sphincter basal pressures greater than 40 mm Hg, and positive analysis for cholesterol and/or calcium bilirubinate crystals). RESULTS: ERCP alone identified a cause of idiopathic recurrent pancreatitis in 47 (37%) patients: papillary stenosis in 26 (21%), pancreas divisum in 9 (7%), and choledocholithiasis in 6 (5%). Among patients with a gallbladder, microcrystals were found in 27 (50%) and sphincter dysfunction in 17 (31%). Among patients who have undergone cholecystectomy, sphincter dysfunction was identified in 24 (47%). Minor papilla sphincterotomy was performed in 8 patients (89%) with pancreas divisum. Biliary sphincterotomy was performed in 85 patients and included all patients with choledocholithiasis, choledochocele, microcrystals, papillary stenosis, and sphincter dysfunction except 2 patients with microcrystals who underwent cholecystectomy. Additionally, pancreatic sphincterotomy was performed in 32 (78%) patients with pancreatic sphincter hypertension and in 6 (23%) of 26 patients with papillary stenosis with dilated pancreatic ducts. Thus, among the 126 patients, 93 of the 100 patients with a detected abnormality underwent endoscopic sphincterotomy. Response rates varied from 67% to 100% during follow-up (mean 29.6 months, range 18 to 33 months). CONCLUSION: ERCP techniques including minor papilla cannulation, analysis of bile for microcrystals, and sphincter of Oddi manometry identified a cause of idiopathic recurrent pancreatitis in 79% (endoscopically treatable in 75%) of patients, with or without prior cholecystectomy.
Adolescent↗
Pathophysiological significance of neuronal nitric oxide synthase in the gastrointestinal tract.
It has been demonstrated that nitric oxide (NO) is a major inhibitory nonadrenergic, noncholinergic (NANC) neurotransmitter in the gastrointestinal (GI) tract. NO released in response to nerve stimulation of the myenteric plexus causes relaxation of the smooth muscle. NO is synthesized by the activation of neuronal NO synthase (nNOS) in the myenteric plexus. Released NO plays an important physiological role in various parts of the GI tract. NO regulates the muscle tone of the sphincter in the lower esophagus, pylorus, sphincter of Oddi, and anus. NO also regulates the accommodation reflex of the fundus and the peristaltic reflex of the intestine. Previous studies have shown that NOS inhibitors delay gastric emptying and colonic transit. The reduction of nNOS expression, associated with impaired local production of NO, may be responsible for motility disorders in the GI tract. There is accumulated evidence that dysfunction of NO neurons in the myenteric plexus may cause various GI diseases. These reports are reviewed and possible mechanisms of altered nNOS expression are discussed in this article. In particular, impaired nNOS synthesis of the myenteric plexus seems to be an important contributing factor to the pathogenesis of achalasia, diabetic gastroparesis, infantile hypertrophic pyloric stenosis, Hirschsprung's disease, and Chagas' disease. Reduced NO release and/or nNOS expression are suspicious in a subset of patients with functional dyspepsia. Although the etiology of intestinal pseudo-obstruction remains unknown, it is conceivable that extrinsic denervation may upregulate nNOS expression, resulting in enhanced muscular relaxation and disturbed peristalsis. An animal model of colitis showed impaired nNOS expression in the colonic myenteric plexus. Antecedent infection may be associated with the impaired NO pathways observed in functional dyspepsia, colitis, and Chagas' disease.
Animals↗
Scintigraphic assessment of SO dysfunction.
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Common Bile Duct Diseases↗
Advances in research and clinical practice in motor disorders of the sphincter of Oddi.
Perfusion manometry of the sphincter of Oddi (SO) using a pneumohydraulic capillary infusion system records phasic wave activity superimposed on basal pressure. A triple-lumen catheter allows the recording of propagation of the phasic waves. Microtransducer manometry is an alternative that permits prolonged recording of biliary pressure without the need for infusion. A cyclic change is recognized in SO motility in coordination with the migrating motor complex (MMC) of the duodenum during fasting. SO contractions occur at maximal frequency and amplitude during phase 3 of the duodenal MMC. Using two microtransducer catheters placed by duodenoscopy, a cyclic elevation of biliary pressure can be recorded in concert with phase 3. These findings indicate that human SO contractions impede bile flow. SO dysfunction causing biliary-type pain can be diagnosed by manometry. The pressure elevation during phase 3 may contribute to the development of pain in patients with biliary dyskinesia. Gastrectomy and proximal duodenal transection were proven to affect sphincter motility, as evidenced by the paradoxical response to cholecystokinin. Choledocholithiasis and hepatolithiasis are associated with low basal pressure, presumably due to repeated injury to the sphincter by passing stones. SO and biliary manometry leads to better understanding of biliary dynamics and the pathophysiology of biliary diseases.
Biliary Dyskinesia↗
Sphincter of Oddi in health and disease.
Sphincter of Oddi (SO) is a dynamic structure located strategically at the confluence of the bile duct, the pancreatic duct and the duodenum. The advent of lateral viewing endoscope along with a minimally compliant pneumocapillary manometry system has greatly enhanced our ability to evaluate the SO in health and disease. These studies have shown that the SO motor function is a complex phenomenon controlled by a variety of neurohumoral agents. The sphincter also actively participates in the Migratory Motor Complex (MMC). The major function of the SO seems to be in regulating the flow of bile and pancreatic juice into the duodenum. By maintaining a basal tone, the sphincter diverts bile into the gallbladder under fasting conditions. On the other hand it functions as "a pump" as well to milk bile into the duodenum. Recent manometric studies also have unravelled a number of abnormalities involving the SO motor function often referred to as SO dysfunction. Most such patients respond favorably to sphincter ablation. Studies are underway to better define patients with SO dysfunction as well as to identify them using noninvasive investigations.
Cholangiopancreatography, Endoscopic Retrograde↗
The effect of h(1) calponin expression on gallstone formation in pregnancy.
OBJECTIVE: To explore the effect of h(1) calponin mRNA expression on the biliary tract dynamics, and investigate the molecular mechanisms of gallstone formation in pregnancy. METHODS: This study was carried out in Renmin Hospital of Wuhan University, and in the Department of Molecular Biology and Biochemistry, Wuhan University School of Medicine, Wuhan, China from July to December 2004. Thirty female guinea pigs were divided randomly into 3 groups, the nonpregnant group (n=10) (group A), the 30 days of pregnancy group (n=10) (group B), and the 60 days of pregnancy group (n=10) (group C). Animal models of pregnancy were established on pregnant group guinea pigs through feeding animals with one cage according to female versus male as 4:1. The total cholesterol (TC), total bilirubin (TBiL), total bile acid (TBA) in the bile and the serum estradiol (E(2)), progesterone (Pg) levels were determined respectively. Expression levels of h(1) calponin mRNA in gallbladder smooth muscles and Oddi's Sphincter (OS) were evaluated using semiquantitative reverse transcription polymerase chain reaction (RT-PCR). RESULTS: The concentration of TC, TBiL and the serum E(2) and Pg were more significantly increasing in group C than that in the other 2 groups. However, the concentration of TBA decreased gradually from group A to group C. Up-regulation of h(1) calponin gene expression was observed in the gallbladder smooth muscles in group C, but converse in OS. CONCLUSION: The h(1) calponin might play an important role in inducing dysfunction of extrahepatic biliary tract, bile stasis in gallbladder and gallstone formation in pregnancy.
Animals↗
The Nardi test and biliary manometry in the diagnosis of pancreaticobiliary sphincter dysfunction.
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Adult↗
Motility of the sphincter of Oddi and pancreatic main ductal pressure in patients with alcoholic, gallstone-associated, and idiopathic chronic pancreatitis.
We endoscopically measured pressures of the pancreatic duct (PP) and the sphincter of Oddi (SO) in patients with alcoholic (ALCP, n = 10), gallstone-associated (GSCP, n = 7), and idiopathic chronic pancreatitis (ICP, n = 21), and in 20 controls. The PP was significantly higher in the patients with ALCP (55.7 +/- 28.9 mm Hg), GSCP (33.6 +/- 16.2 mm Hg), or ICP (44.5 +/- 25.8 mm Hg) than in the controls (16.2 +/- 8.7 mm Hg), but there was no significant difference between ALCP, GSCP, and ICP. There was no significant difference between control subjects and ICP in the motility of SO. In ICP, there was no correlation between the PP and the motility of SO. In ALCP and GSCP, the frequencies of the papillary sphincter waves were significantly higher than in normal subjects, and there were correlations between the PP and the motility of SO. These data suggest that increased pancreatic ductal pressure in GSCP with papillitis or ALCP may be due in part to papillary dysfunction, but not in ICP.
Alcoholism↗
Endoscopic manometry of the sphincter of Oddi in patients with Lemmel's syndrome.
Endoscopic manometry was performed to evaluate the motor activity of the sphincter of Oddi (OS) in six patients with Lemmel's syndrome, four of whom had acute cholangitis and two of whom had acute pancreatitis. As controls, 24 patients undergoing cholecystectomy without juxtapapillary duodenal diverticula (JPD) for cholelithiasis or cholesterol polyps in the gallbladder were also studied. The OS basal pressure and contraction pressure values were 12.4 +/- 5.1 mmHg and 103.4 +/- 24.3 mmHg, respectively, in the patients with Lemmel's syndrome, and 19.5 +/- 5.1 mmHg and 136.8 +/- 28.2 mmHg, respectively, in the control patients. These differences between the groups were statistically significant; however, the wave frequency was not significantly different between the groups. The mean percentages of antegrade, simultaneous, and retrograde sequences were 37.5% +/- 11.3%, 19.9% +/- 8.7%, and 43.4% +/- 11.7%, respectively, in the patients with Lemmel's syndrome, and 66.5% +/- 11.0%, 20.2% +/- 4.7%, and 14.3% +/- 9.2%, respectively, in the controls. The differences between the groups were significant (P < 0.01) for the antegrade and retrograde sequences. These findings indicate that dysfunction of the OS in patients with Lemmel's syndrome could be important in the development of hepatocholangiopancreatic disease caused by duodenobiliary and duodenopancreatic reflux.
Acute Disease↗