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Journal articles on the topic 'Sphincter of Oddi'

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Published: 4 June 2021

Last updated: 29 January 2023

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1

Thune, A., L. Jivegård, H. Pollard, J. Moreau, J. C. Schwartz, and J. Svanvik. "Location of enkephalinase and functional effects of [Leu5] enkephalin and inhibition of enkephalinase in the feline main pancreatic and bile duct sphincters." Clinical Science 82, no. 2 (February 1, 1992): 169–73. http://dx.doi.org/10.1042/cs0820169.

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1. Morphological studies have demonstrated enkephalinergic nerve fibres in proximity to the sphincter of Oddi, and opiates are known to contract this sphincter. In this study, the flow resistances in the common bile duct and main pancreatic duct sphincters were studied simultaneously in anaesthetized cats using a perfusion technique. 2. Naloxone did not affect the activity of these sphincters under basal conditions, indicating that there is no basal enkephalinergic tone. 3. The response to [Leu5]enkephalin (0.015–15 μg/kg), morphine (1 mg/kg) and ketamine (10 mg/kg) was a naloxone-sensitive increased activity in the sphincters with a raised frequency of phasic contractions. The threshold dose for an effect of [Leu5]enkephalin on the sphincter of Oddi was 0.015 μg/kg and a maximal response was observed at 0.75 μg/kg. There were no differences in the response of the main pancreatic duct sphincter and the bile duct sphincter to the different drugs. 4. Immunoautoradiographic studies demonstrated enkephalinase in the spincter of Oddi. 5. Acetorphan (3 mg/kg intravenously), which inhibits endogenous enkephalinase both in the peripheral and the central nervous system when administered parenterally, caused a naloxone-sensitive contraction, whereas thiorphan (3–20 mg/kg), an enkephalinase inhibitor that does not easily penetrate the blood-brain barrier, had no effect on the sphincter of Oddi. 6. These results show that endogenous and exogenous opiates influence the function of the feline sphincter of Oddi and that enkephalins may be involved in the physiological control of this sphincter, although not under basal conditions.

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2

Lehman, Glen A., and Stuart Sherman. "Hypertensive Pancreatic Sphincter." Canadian Journal of Gastroenterology 12, no. 5 (1998): 333–37. http://dx.doi.org/10.1155/1998/148150.

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Major papilla pancreatic sphincter dysfunction, a variant of sphincter of Oddi dysfunction, causes pancreatitis or pancreatic-type pain. Endoscopic manometry as performed at endoscopic retrograde cholangiography is the most commonly used method to identify sphincter dysfunction. Noninvasive testing, such as secretin-stimulated ultrasound analysis of duct diameter, is less reliable and of relatively low sensitivity. Two-thirds of patients with sphincter of Oddi dysfunction have elevated pancreatic basal sphincter pressure. Patients with suspected or documented sphincter of Oddi dysfunction may respond to biliary sphincterotomy alone, but warrant evaluation of their pancreatic sphincter if symptoms persist after therapy. Whether such pancreatic and biliary sphincters should be treated at the first treatment session is controversial. Pancreatic sphincterotomy is associated with a complication rate very similar to that of biliary sphincterotomy except that the pancreatitis rate is two- to fourfold higher. Prophylactic pancreatic stenting diminishes such pancreatitis by approximately 50%.

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3

Haubrich, William S. "Oddi of the sphincter of Oddi." Gastroenterology 116, no. 3 (March 1999): 542. http://dx.doi.org/10.1016/s0016-5085(99)70217-9.

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4

Polunina, T. E. "Sphincter of Oddi dysfunction. Case history." Medical Council, no. 3 (May 12, 2019): 26–33. http://dx.doi.org/10.21518/2079-701x-2019-3-26-33.

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The article presents the definition and prevalence of sphincter of Oddi dysfunction in patients with various disorders of the biliary system. It describes the characteristics of sphincter of Oddi dysfunction with due account of its anatomical structure. Based on Rome IV Criteria (2016), the authors provide modern approaches to the diagnosis and treatment of sphincter of Oddi dysfunction. Special attention is paid to the diagnostic criteria for sphincter of Oddi dysfunction depending on its type. There are two basic types of sphincter of Oddi dysfunction: biliary dysfunction and pancreatitis. The paper presents the algorithms for the examination and treatment of patients with sphincter of Oddi dysfunction depending on the severity level of the disease and objective findings of laboratory and instrumental tests. The article presents a clinical history of a patient with sphincter of Oddi dysfunction. Depending on the characteristics of a clinical course of dysfunction, it was proposed that the patient was treated with a selective antispasmodic drug and a choleretic drug.

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5

Della Libera, Ermelindo, Rodrigo Azevedo Rodrigues, Ana Paula Rodrigues Guimarães, Gustavo Andrade de Paulo, Stephan Geocze, and Angelo Paulo Ferrari. "Prevalence of sphincter of Oddi dysfunction in patients referred to endoscopic retrograde cholangiopancreatography." Arquivos de Gastroenterologia 44, no. 1 (March 2007): 18–21. http://dx.doi.org/10.1590/s0004-28032007000100005.

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BACKGROUND: Sphincter of Oddi manometry is the gold-standard method for sphincter of Oddi dysfunction. The prevalence of sphincter of Oddi dysfunction among patients referred to endoscopic retrograde cholangiopancreatography is largely unknown. AIM: To evaluate prospectively the prevalence of biliary sphincter of Oddi dysfunction (B-SOD) among Brazilian patients referred to endoscopic retrograde cholangiopancreatography and to study the safety of sphincter of Oddi manometry in this setting. METHODS: Biliary sphincter of Oddi manometry was intended in 110 patients referred to endoscopic retrograde cholangiopancreatography. The number of attempts to obtain deep cannulation with the manometry catheter was recorded and patients were divided into two groups: up to 5 (easy cannulation) and >5 attempts (difficult cannulation). RESULTS: Sphincter of Oddi manometry was successful in 71/110 patients (64.5%). Sphincter of Oddi dysfunction was found in 18/71 patients (25%). Endoscopic retrograde cholangiopancreatography findings were: normal in 16, biliary stones in 39, malignant biliary strictures in 9 and benign biliary strictures in 7. There was no statistical difference in sphincter of Oddi dysfunction prevalence regarding disease, gender or difficulty of cannulation. Only 2/71 patients developed post-procedure mild pancreatitis. CONCLUSIONS: We have found a high prevalence of sphincter of Oddi dysfunction in patients referred to endoscopic retrograde cholangiopancreatography. Gender, nature of disease or difficulty of cannulation did not influence the prevalence of sphincter of Oddi dysfunction among these patients. Sphincter of Oddi manometry is a safe procedure for the evaluation of sphincter of Oddi dysfunction in patients referred to endoscopic retrograde cholangiopancreatography.

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6

Zhang, Qi, Mao Ye, Wei Su, Yiwen Chen, Yu Lou, Jiaqi Yang, Tao Ma, et al. "Normal sphincter of Oddi." ASVIDE 7 (November 2020): 274. http://dx.doi.org/10.21037/asvide.2020.274.

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7

Zhang, Qi, Mao Ye, Wei Su, Yiwen Chen, Yu Lou, Jiaqi Yang, Tao Ma, et al. "Lax sphincter of Oddi." ASVIDE 7 (November 2020): 275. http://dx.doi.org/10.21037/asvide.2020.275.

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8

Funch-Jensen, P., and N. Ebbehøj. "Sphincter of Oddi Motility." Scandinavian Journal of Gastroenterology 31, sup216 (January 1996): 46–51. http://dx.doi.org/10.3109/00365529609094560.

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9

Lehman, Glen A., and Stuart Sherman. "Sphincter of Oddi dysfunction." International Journal of Pancreatology 20, no. 1 (August 1996): 11–25. http://dx.doi.org/10.1007/bf02787372.

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10

Boivineau, G., J. M. Gonzalez, M. Gasmi, V. Vitton, and M. Barthet. "Sphincter of Oddi dysfunction." Journal of Visceral Surgery 159, no. 1 (March 2022): S16—S21. http://dx.doi.org/10.1016/j.jviscsurg.2022.01.008.

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11

Hyun, Jong Jin, and Richard A. Kozarek. "Sphincter of Oddi dysfunction." Current Opinion in Gastroenterology 34, no. 5 (September 2018): 282–87. http://dx.doi.org/10.1097/mog.0000000000000455.

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12

Corazziari, E. "Sphincter of Oddi dysfunction." Digestive and Liver Disease 35 (July 2003): 26–29. http://dx.doi.org/10.1016/s1590-8658(03)00090-2.

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13

ORFORD, JAMES L., PABLO E. DIBOS, and GABRIEL SOUDRY. "Sphincter of Oddi Dysfunction." Clinical Nuclear Medicine 25, no. 9 (September 2000): 670–75. http://dx.doi.org/10.1097/00003072-200009000-00003.

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14

Cox, Alan J., Stephen A. McClave, Mark H. Bronner, Warren Kemper, and Richard A. Wright. "SPHINCTER OF ODDI MOTILITY." Southern Medical Journal 85, Supplement (September 1992): 3S—37. http://dx.doi.org/10.1097/00007611-199209001-00095.

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15

KIMMEY, M., F. ALKAWAS, D. CARRLOCKE, S. EDMUNDOWICZ, R. GANNAN, P. JAMIDAR, Z. SAEED, and T. STEIN. "Sphincter of oddi manometry." Gastrointestinal Endoscopy 43, no. 2 (1996): 645–46. http://dx.doi.org/10.1016/s0016-5107(96)81614-2.

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16

Pfau, Patrick R., Subhas Banerjee, Bradley A. Barth, David J. Desilets, Vivek Kaul, Sripathi R. Kethu, Marcos C. Pedrosa, et al. "Sphincter of Oddi manometry." Gastrointestinal Endoscopy 74, no. 6 (December 2011): 1175–80. http://dx.doi.org/10.1016/j.gie.2011.07.055.

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17

Baillie, John. "Sphincter of Oddi Dysfunction." Current Gastroenterology Reports 12, no. 2 (March 10, 2010): 130–34. http://dx.doi.org/10.1007/s11894-010-0096-1.

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18

Funch-Jensen, Peter. "Sphincter of Oddi physiology." Journal of Hepato-Biliary-Pancreatic Surgery 2, no. 3 (September 1995): 249–54. http://dx.doi.org/10.1007/bf02350906.

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19

Bosch, Antonio, and Luis R. Peña. "The Sphincter of Oddi." Digestive Diseases and Sciences 52, no. 5 (March 14, 2007): 1211–18. http://dx.doi.org/10.1007/s10620-006-9171-8.

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20

Small, Aaron J., and Richard A. Kozarek. "Sphincter of Oddi Dysfunction." Gastrointestinal Endoscopy Clinics of North America 25, no. 4 (October 2015): 749–63. http://dx.doi.org/10.1016/j.giec.2015.06.009.

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21

Menees, Stacy, and Grace H. Elta. "Sphincter of oddi dysfunction." Current Treatment Options in Gastroenterology 8, no. 2 (April 2005): 109–15. http://dx.doi.org/10.1007/s11938-005-0003-2.

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22

Elta, G. H. "Sphincter of Oddi manometry in patients with possible sphincter of Oddi dysfunction." Gastroenterology 101, no. 6 (December 1991): 1747–48. http://dx.doi.org/10.1016/0016-5085(91)90423-i.

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23

Lehman, G. A. "Sphincter of Oddi manometry in patients with possible sphincter of Oddi dysfunction." Gastroenterology 101, no. 6 (December 1991): 1748. http://dx.doi.org/10.1016/0016-5085(91)90424-j.

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24

Muller, E. L., P. A. Grace, R. L. Conter, J. J. Roslyn, and H. A. Pitt. "Influence of motilin and cholecystokinin on sphincter of Oddi and duodenal mobility." American Journal of Physiology-Gastrointestinal and Liver Physiology 253, no. 5 (November 1, 1987): G679—G683. http://dx.doi.org/10.1152/ajpgi.1987.253.5.g679.

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The sphincter of Oddi and the duodenum exhibit cyclical activity in phase with the migrating myoelectric complex. Both motilin and cholecystokinin have been shown to modulate gastrointestinal and sphincter of Oddi motility. However, previous studies have not monitored the effects of these hormones on simultaneously recorded sphincter of Oddi and duodenum pressures. The present investigation was undertaken, therefore, to determine the influence of both motilin and cholecystokinin on simultaneously recorded sphincter of Oddi and duodenal motility. In seven anesthetized prairie dogs, a triple-lumen, side-hole, pressure-monitored perfusion catheter was positioned with the proximal port in the sphincter of Oddi and the distal port in the duodenal lumen. Sphincter of Oddi and duodenal motility was recorded before and during 20-min infusions of motilin and cholecystokinin octapeptide (CCK-8) at 1, 10, and 100 ng.kg-1.min-1. Both hormones produced dose-related increases in sphincter of Oddi and duodenal motility. No response was observed with either hormone at 1 ng.kg-1.min-1. At 10 ng.kg-1.min-1, the duodenum was slightly more sensitive to motilin than to CCK-8, while the sphincter of Oddi was equally affected by both hormones. At 100 ng.kg-1.min-1, both hormones stimulated the sphincter of Oddi and the duodenum equally. These data indicate that in the prairie dog, both motilin and cholecystokinin stimulate sphincter of Oddi and duodenal motility.

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25

DAVIS, MARILEE. "Physiology of the Human Sphincter of Oddi; Pharmacology of the Sphincter of Oddi." Radiology 174, no. 1 (January 1990): 146. http://dx.doi.org/10.1148/radiology.174.1.146.

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26

Haider, Asim, Ayesha Siddiqa, Nisha Ali, and Shehriyar Mehershahi. "Biliary Sphincter of Oddi Dysfunction." Case Reports in Gastroenterology 15, no. 1 (April 28, 2021): 443–49. http://dx.doi.org/10.1159/000514542.

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Sphincter of Oddi dysfunction (SOD) is a syndrome caused by either dyskinesia or stenosis of the sphincter of Oddi. It has been categorized into biliary and pancreatic SOD based on clinical features and laboratory findings. We present a case of a 51-year-old female (post-cholecystectomy) who presented with intermittent chronic right upper quadrant pain. Laboratory investigations showed persistently elevated liver function tests and a dilated common bile duct without the presence of any stones. Endoscopic retrograde cholangiopancreatography with manometry showed an elevated sphincter of Oddi pressure, thus confirming the diagnosis of SOD. She underwent endoscopic sphincterotomy and papillotomy with normalization of liver function tests and resolution of her chronic symptoms.

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27

Harling, Henrik, Tina Messell, Steen Lindkaer Jensen, and Steen Seier Poulsen. "Distribution and Effect of Galanin on Gallbladder and Sphincter of Oddi Motility in the Pig." HPB Surgery 3, no. 4 (January 1, 1991): 279–89. http://dx.doi.org/10.1155/1991/20383.

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This study was designed to determine the occurrence and topographical distribution of galanin-like immunoreactivity (GAL-LI) in the porcine gallbladder and sphincter of Oddi and to investigate the pharmacologic effect of GAL on gallbladder and sphincter of Oddi motility. By radioimmunoassay the concentration of GAL-LI in the gallbladder was 2.75 ± 0.23, 9.73 ± 1.33 in the common bile duct and 5.10 ± 0.37 in the sphincter of Oddi (pmol/g ± SE). By immunohistochemistry GAL-LI was found exclusively in ganglionic cells and in nerve fibers among the smooth muscle bundles. Gallbladder and sphincter of Oddi pressures were recorded before and during 5-minute local intraarterial infusion of 4, 8, 19, 39, 78 and 194 ng GAL-Kg-1-min-1 in 12 anaesthetized pigs. GAL in doses ≥ 39 ng.kg-1.min-1 significantly reduced sphincter of Oddi phasic wave frequency (4.8 ± 0.4 vs. 2.1 ± 0.5; p = 0.004) and sphincter of Oddi motility index (70.2 ± 6.02 vs. 27.7 ± 8.3; p = 0.002) but did not affect gallbladder pressure. We conclude that the distribution of GAL-LI in the sphincter of Oddi and the effect that a pharmacologic dose of GAL has on sphincter of Oddi motor activity, suggests that GAL may be involved in the physiologic control of bile flow in the pig.

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28

Harrington, Karen, Arieh Bomzon, Keith A. Sharkey, Joseph S. Davison, and Eldon A. Shaffer. "Differential sensitivities of the sphincter of Oddi and gallbladder to cholecystokinin in the guinea pig: their role in transsphincteric bile flow." Canadian Journal of Physiology and Pharmacology 70, no. 10 (October 1, 1992): 1336–41. http://dx.doi.org/10.1139/y92-187.

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Cholecystokinin (CCK) is considered to simply contract the gallbladder and relax the sphincter of Oddi with meals. In this study, we examined this hypothesis by investigating the action of CCK on the sphincter of Oddi and gallbladder of the guinea pig. The experimental design used an in vitro preparation of the sphincter of Oddi to measure contraction of the circular muscle. CCK increased tone in both the gallbladder and the sphincter of Oddi in a concentration-dependent manner. The normalized concentration–response curves for CCK, however, revealed that the gallbladder had a greater sensitivity to CCK (ED50 7 nM) than the sphincter of Oddi (ED50 22 nM; p < 0.01). Conversely, the sphincter was more sensitive to bethanechol than was the gallbladder. When the sphincter of Oddi was stimulated maximally with CCK in the presence of atropine (10−6 M) or tetrodotoxin (10−6 M), the contractile response was significantly reduced (p < 0.05) although not abolished. Conversely, atropine completely abolished the responses to bethanechol (10−3 M) and transmural field stimulation (70 V, 10 Hz, 1 ms, for 20 s). Transmural field stimulation of the sphincter that had been precontracted with CCK (26 nM) caused a transient, initial relaxation followed by contraction. Pretreatment with atropine augmented the duration of this relaxation, which could be completely abolished by tetrodotoxin. Thus, CCK contracts the sphincter of Oddi in the guinea pig by a direct (myogenic) and a neural (likely cholinergic) mechanism. Relaxation of the sphincter of Oddi also occurs in the guinea pig via noncholinergic inhibitory nerves. Duodenal delivery of bile is expedited by CCK, which induces gallbladder contraction at low, near-physiological levels without stimulating the sphincter. Under other conditions, sphincter of Oddi relaxation may facilitate transsphincteric flow. In contrast, increased cholinergic tone may help prevent duodenal reflux into the biliary system.Key words: cholecystokinin, bethanechol, enteric nervous system, gallbladder function, sphincter of Oddi.

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29

Toouli, James, and Alexander Craig. "Sphincter of Oddi Function and Dysfunction." Canadian Journal of Gastroenterology 14, no. 5 (2000): 411–19. http://dx.doi.org/10.1155/2000/313601.

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The sphincter of Oddi (SO) is situated at the junction of the bile and pancreatic ducts where they enter the duodenum, and it serves to regulate the flow of bile and pancreatic juices as well as to prevent the reflux of duodenal contents into the pancreatobiliary system. SO dysfunction relates to either the biliary or pancreatic portions of the sphincter. Distinct clinical syndromes relating to either sphincter segment are recognized. The mechanism of dysfunction remains uncertain, but disruption of neural pathways involved in sphincter function seems likely. SO dysfunction is best diagnosed by manometry, which is able to correctly stratify patient groups and determine therapy. Biliary scintigraphy, which is noninvasive, has shown promise as a screening tool for patients with suspected SO dysfunction. Division of the sphincter is an effective treatment for patients with manometrically proven SO stenosis for either the biliary or pancreatic form of the disorder. Other forms of SO dysfunction may benefit from pharmacotherapy.

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30

Cullen, J. J., B. M. Herrmann, R. M. Thomas, S. Fang, J. A. Murray, A. Ledlow, J. Christensen, and J. L. Conklin. "The role of antioxidant enzymes in the control of opossum sphincter of Oddi motility." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 5 (May 1, 1997): G1050—G1056. http://dx.doi.org/10.1152/ajpgi.1997.272.5.g1050.

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Superoxide rapidly oxidizes nitric oxide (NO) to form peroxynitrite, thus terminating the biological activity of NO. The aims of our study were to determine if superoxide alters the motor function of the sphincter of Oddi and to localize the antioxidant enzymes in the sphincter of Oddi. Immunostaining was performed and enzyme activities were measured in the sphincter of Oddi. In physiological experiments, force-displacement transducers recorded tension in the spontaneously contracting sphincter of Oddi and after electrical field stimulation (EFS) of precontracted sphincter of Oddi. Superoxide was generated by the addition of xanthine with xanthine oxidase, superoxide radicals were scavenged by the addition of superoxide dismutase (SOD), and catalase or SOD was inhibited by diethyldithiocarbamic acid. Immunostaining demonstrated SOD and catalase immunoreactivity in ganglia situated at the serosal surface of the circular muscle. Total SOD activity was 202 +/- 12 U/mg. Generation of superoxide or inhibition of SOD increased the contractile frequency and decreased relaxation after EFS. We conclude that superoxide alters sphincter of Oddi motor function, and the presence of superoxide scavenging enzymes in enteric plexuses suggests that they may regulate sphincter of Oddi neuromuscular function by clearing endogenous superoxide.

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31

Rice, John P., Bret J. Spier, Deepak V. Gopal, Anurag Soni, Mark Reichelderfer, and Patrick R. Pfau. "Outcomes of Sphincter of Oddi Manometry When Performed in Low Volumes." Diagnostic and Therapeutic Endoscopy 2011 (June 2, 2011): 1–5. http://dx.doi.org/10.1155/2011/435806.

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Background. Sphincter of Oddi manometry is a highly specialized procedure associated with an increased risk of procedural complications. Published studies have typically been performed in large volume manometry centers. Objective. To examine the outcomes and complication rate of SOM when performed in small volumes. Design. Retrospective analysis at a tertiary care referral hospital that infrequently performs Sphincter of Oddi manometry. Patient records were reviewed for procedural details, patient outcomes, and complications after sphincter of Oddi manometry. Results. 36 patients, 23 (23 type II sphincter of Oddi dysfunction (SOD), 13 type III SOD) underwent sphincter of Oddi manometry and were followed up for mean of 16 months. Nine Type II patients (90%) with elevated basal sphincter pressures noted symptom improvement after sphincterotomy compared with only 3 patients (43%) of the patients with normal basal pressures. In type III SOD, 7 patients had elevated basal SO pressure and underwent sphincterotomy. Three patients (43%) improved. There were six (16%) procedure-related complications. There were four cases of post ERCP pancreatitis (11%), all of which were mild. Conclusion. In low numbers, sphincter of Oddi manometry can be performed successfully and safely by experienced biliary endoscopists with results that are comparable to large volume centers.

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32

Han, Jimin, and Ho Gak Kim. "Pancreatic Sphincter of Oddi Dysfunction." Korean Journal of Gastroenterology 53, no. 6 (2009): 333. http://dx.doi.org/10.4166/kjg.2009.53.6.333.

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33

Heetun, Zaid S., Faisal Zeb, Garrett Cullen, Garry Courtney, and Abdur Rahman Aftab. "Biliary sphincter of Oddi dysfunction." European Journal of Gastroenterology & Hepatology 23, no. 4 (April 2011): 327–33. http://dx.doi.org/10.1097/meg.0b013e3283433aa1.

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34

Funch-Jensen, Peter. "Defining Sphincter of Oddi Dysfunction." Gastrointestinal Endoscopy Clinics of North America 6, no. 1 (January 1996): 107–15. http://dx.doi.org/10.1016/s1052-5157(18)30380-5.

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35

Schulze-Delrieu, K. "Oddi-ties of sphincter contractions." Gastroenterology 90, no. 6 (June 1986): 2030. http://dx.doi.org/10.1016/0016-5085(86)90283-0.

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36

Tanaka, Masao, Norbert Senninger, Norbert Runkel, and Christian Herfarth. "Sphincter of Oddi cyclic motility." Gastroenterology 98, no. 2 (February 1990): 347–52. http://dx.doi.org/10.1016/0016-5085(90)90824-k.

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37

Goff, John S. "The Human Sphincter of Oddi." Archives of Internal Medicine 148, no. 12 (December 1, 1988): 2673. http://dx.doi.org/10.1001/archinte.1988.00380120115023.

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38

Ahrendt, S. A., G. M. Ahrendt, K. D. Lillemoe, and H. A. Pitt. "Effect of octreotide on sphincter of Oddi and gallbladder motility in prairie dogs." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 5 (May 1, 1992): G909—G914. http://dx.doi.org/10.1152/ajpgi.1992.262.5.g909.

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Somatostatin and its synthetic analogue, octreotide, inhibit gallbladder emptying and cause gallstones. Whether octreotide-induced alterations in sphincter of Oddi motility contribute to this process is unknown. We, therefore, examined the effect of octreotide on fasting and protein-stimulated sphincter of Oddi motility. In 25 anesthetized prairie dogs, sphincter of Oddi motility and gallbladder pressure were monitored during the intravenous administration of octreotide, cholecystokinin (CCK) octapeptide, atropine, the intraduodenal administration of casein, and combinations of these agents. Intravenous octreotide decreased fasting sphincter of Oddi motility index both with (59 +/- 19 vs. 84 +/- 28, P less than 0.05) and without (137 +/- 31 vs. 227 +/- 42, P less than 0.05) prior cholinergic blockade with atropine. Octreotide also prevented the increases in sphincter of Oddi motility and gallbladder pressure seen with intraduodenal casein. Exogenous CCK increased sphincter of Oddi motility index and gallbladder pressure despite the simultaneous administration of octreotide alone (357 +/- 109 vs. 137 +/- 31, P less than 0.07, and 11.2 +/- 1.0 mmHg vs. 9.6 +/- 0.6 mmHg, P less than 0.05) or the combination of octreotide and atropine (317 +/- 69 vs. 59 +/- 19, P less than 0.05, and 10.1 +/- 1.6 mmHg vs. 8.5 +/- 1.4 mmHg, P less than 0.05). We conclude that both a cholinergic and an octreotide-sensitive noncholinergic pathway stimulate fasting sphincter of Oddi motility in the prairie dog.

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39

Toyoyama, Hirokatsu, Nobutaka Kariya, Ichiro Hase, and Yoshiro Toyoda. "The Use of Intravenous Nitroglycerin in a Case of Spasm of the Sphincter of Oddi during Laparoscopic Cholecystectomy." Anesthesiology 94, no. 4 (April 1, 2001): 708–9. http://dx.doi.org/10.1097/00000542-200104000-00027.

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Spasm of the sphincter of Oddi still occurs during cholecystectomy. Some reports indicate that the spasm, induced by morphine, can be reversed by injection of naloxone, nalbuphine, and glucagon. Others maintain that nitroglycerin or nifedipine can relax the sphincter of Oddi muscle. We recently encountered spasm of the sphincter of Oddi during a laparoscopic cholecystectomy and treated it successfully with intravenous nitroglycerin.

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40

Sievert, C. E., T. J. Potter, A. S. Levine, J. E. Morley, S. E. Silvis, and J. A. Vennes. "Effect of bombesin and gastrin-releasing peptide on canine sphincter of Oddi." American Journal of Physiology-Gastrointestinal and Liver Physiology 254, no. 3 (March 1, 1988): G361—G365. http://dx.doi.org/10.1152/ajpgi.1988.254.3.g361.

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This study reports the effects of bombesin and gastrin-releasing peptide (GRP) on the canine sphincter of Oddi using a method that allows repeated cannulation of the biliary sphincter in the unanesthetized animal through a Thomas cannula placed opposite the biliary papilla. Immediately after intravenous administration of bombesin or GRP, phasic sphincter contractions disappeared, basal sphincter pressures fell, and common bile duct pressures rose. Because bombesin releases cholecystokinin (CCK) and CCK resulted in a similar pattern to that of bombesin, the bombesin effect on the sphincter of Oddi may have been secondary to CCK's effect on the sphincter. To test if the bombesin effect on the sphincter of Oddi was due to the release of CCK, we blocked CCK release by administration of somatostatin, having first established that somatostatin blocked endogenous CCK release in our animal model by use of an intraduodenal infusion of lipid. Exogenous administration of bombesin failed to alter sphincter of Oddi or common bile duct pressures in dogs treated with somatostatin. Somatostatin did not, however, block CCK's effect on gallbladder contraction, since exogenous administration of CCK after somatostatin injection resulted in the pressure changes in the biliary tree typical of CCK-induced gallbladder contraction. Thus bombesin administration appears to result in sphincter relaxation and gallbladder contraction by the release of endogenous CCK rather than by a direct effect. The increase in common bile duct pressures was due to gallbladder contraction, since this rise in pressure was abolished by cholecystectomy. The peptide effect on sphincter contraction and basal sphincter pressure were unaffected by cholecystectomy.

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Kalaitzakis, Evangelos, Tim Ambrose, Jane Phillips-Hughes, Jane D. Collier, and Roger W. Chapman. "T1549: Management of Patients With Biliary Sphincter of Oddi Disorder Without Sphincter of Oddi Manometry." Gastrointestinal Endoscopy 71, no. 5 (April 2010): AB306. http://dx.doi.org/10.1016/j.gie.2010.03.761.

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42

Tierney, S., Z. Qian, B. Yung, P. A. Lipsett, H. A. Pitt, S. Sostre, and K. D. Lillemoe. "Gender influences sphincter of Oddi response to cholecystokinin in the prairie dog." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 4 (October 1, 1995): G476—G480. http://dx.doi.org/10.1152/ajpgi.1995.269.4.g476.

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Although gallstones and disorders of biliary tract motility are both more common in women than men, sphincter of Oddi motility has not previously been compared between the sexes. In this study, cholescintigraphy (under ketamine and diazepam anesthesia) was used to determine gallbladder emptying rate and ejection fraction in response to cholecystokinin (CCK) in eight male and six female prairie dogs fed a nonlithogenic diet. Ten days later, under alpha-chloralose anesthesia, sphincter of Oddi phasic wave activity was monitored for 10-min intervals before (control), during 20 min of CCK infusion, and for 20 min after infusion. Gallbladder emptying rate and ejection fraction and baseline sphincter of Oddi frequency, amplitude, and motility index (= frequency x amplitude) did not differ significantly between the sexes. Sphincter of Oddi phasic wave frequency was increased during CCK infusion in both males and females, but the change in amplitude was significantly greater in females, than males. We conclude that the increased incidence of biliary tract disease in women may be due to altered sphincter of Oddi hormonal response.

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Baron, T. H., C. B. Dalton, P. B. Cotton, G. R. May, L. G. Milton, R. S. Chari, and W. C. Meyers. "The Effect of Propofol on the Canine Sphincter of Oddi." HPB Surgery 7, no. 4 (January 1, 1994): 297–304. http://dx.doi.org/10.1155/1994/78764.

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To assess the effect of propofol on the canine sphincter of Oddi (SO), sphincter of Oddi manometry (SOM) was performed in fasting dogs which had undergone cholecystectomy and placement of modified Thomas duodenal cannulae. Using two water-perfused, single-lumen manometric catheters, SO and duodenal pressures were measured simultaneously. Baseline SO activity was recorded for at least one complete interdigestive cycle followed by bolus injections of propofol (Diprivan ®) (N = 31) from 0.1 to 4.0 mg/kg during Phase I of the Migrating Motor Complex (MMC).When propofol was administered in bolus doses ≤ 0.5 mg/kg, no change in SO or duodenal motor function was seen. In doses ≥ 0.5 mg/kg, SO basal pressure, amplitude, and frequency of contractions increased significantly. Increases in duodenal activity paralleled SO activity. Our results suggest that propofol in low doses may be useful for sedation during Sphincter of Oddi manometry in humans. Further studies of the effects of propofol on the human sphincter of Oddi are warranted.

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Scott, R. B., S. C. Diamant, and G. R. Greenberg. "Do motilin and pancreatic polypeptide regulate duodenal bile acid delivery?" Canadian Journal of Physiology and Pharmacology 66, no. 12 (December 1, 1988): 1499–504. http://dx.doi.org/10.1139/y88-245.

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The plasma levels of the enteric hormones, motilin and pancreatic polypeptide, cycle in association with fasting intestinal motility and are altered by feeding. Intravenous administration of motilin causes gallbladder contraction and increased sphincter of Oddi phasic motor activity, whereas pancreatic polypeptide causes gallbladder relaxation. To determine if endogenous plasma levels of motilin and pancreatic polypeptide control sphincter of Oddi and gallbladder motility, and regulate duodenal bile acid delivery, we measured during fasting and after feeding the correlation between (a) changes in plasma motilin or pancreatic polypeptide, and (b) the duodenal delivery of a steady-state hepatic output of radiolabelled bile acid. Four dogs were prepared with duodenal cannulas. Duodenal motility was recorded manometrically. Plasma levels of pancreatic polypeptide and motilin were determined during a full cycle of the migrating myoelectric complex for 20 min before and 40 min after ingestion of a standard meal. To assess the effect of the sphincter of Oddi and the gallbladder together, or the gallbladder alone on duodenal bile acid delivery, the dogs received a continuous i.v. infusion of [14C]taurocholic acid (TCA); duodenal delivery of TCA was quantitated with the sphincter of Oddi intact using duodenal marker perfusion, or with the sphincter of Oddi cannulated and zero outflow resistance. In the interdigestive period with the sphincter of Oddi intact, only 0.1 (r2) of the variance of duodenal bile acid delivery can be predicted from the variance of motilin, and the correlation of plasma pancreatic polypeptide with duodenal TCA delivery is opposite that expected if pancreatic polypeptide caused gallbladder relaxation. In the interdigestive period with the sphincter of Oddi cannulated, or in the postprandial period with the sphincter of Oddi intact or cannulated, the correlations of plasma motilin and pancreatic polypeptide with duodenal TCA delivery are opposite those expected if motilin induces gallbladder contraction, and pancreatic polypeptide induces gallbladder relaxation. Assuming these mechanisms, a causal association between variation in plasma motilin or pancreatic polypeptide and interdigestive or postprandial duodenal bile acid delivery is unlikely.

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McLoughlin, MT. "Sphincter of Oddi dysfunction and pancreatitis." World Journal of Gastroenterology 13, no. 47 (2007): 6333. http://dx.doi.org/10.3748/wjg.v13.i47.6333.

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Rodrigues, Gabriel, and Prasad Seetharam. "Sphincter of Oddi and its dysfunction." Saudi Journal of Gastroenterology 14, no. 1 (2008): 1. http://dx.doi.org/10.4103/1319-3767.37793.

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ONO, Keiichi. "Surgery of the sphincter of Oddi." Japanese Journal of Gastroenterological Surgery 20, no. 3 (1987): 671–79. http://dx.doi.org/10.5833/jjgs.20.671.

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Staritz, M. "Pharmacology of the Sphincter of Oddi." Endoscopy 20, S 1 (September 1988): 171–74. http://dx.doi.org/10.1055/s-2007-1018170.

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Parodi, J. E., and J. M. Becker. "Gallbladder and sphincter of Oddi motility." Current Opinion in Gastroenterology 6, no. 5 (October 1990): 668–76. http://dx.doi.org/10.1097/00001574-199010000-00003.

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Toouli, J. "EVALUATION OF SPHINCTER OF ODDI FUNCTION." ANZ Journal of Surgery 59, no. 6 (June 1989): 445–48. http://dx.doi.org/10.1111/j.1445-2197.1989.tb01608.x.

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