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The sphincter of Oddi (SO) is a smooth muscle valve regulating the flow of biliary and pancreatic secretions into the duodenum, initially described in 1887 by the Italian anatomist, Ruggero Oddi. SO dysfunction (SOD) is a broad term referring to numerous biliary, pancreatic, and hepatic disorders resulting from spasms, strictures, and relaxation of this valve at inappropriate times. This review brings attention to various factors that may increase the risk of SOD, including but not limited to: cholecystectomy, opiates, and alcohol. Lack of proper recognition and treatment of SOD may be associated with clinical events, including pancreatitis and biliary symptoms with hepatic enzyme elevation. Pharmacologic and non-pharmacologic approaches are discussed to help recognize, prevent, and treat SOD. Future studies are needed to assess the treatment benefit of agents such as calcium-channel blockers, glyceryl trinitrate, or tricyclic antidepressants in patients with SOD.

The sphincter of Oddi (SO) is a smooth muscle valve regulating the flow of biliary and pancreatic secretions into the duodenum, initially described in 1887 by the Italian anatomist, Ruggero Oddi. SO dysfunction (SOD) is a broad term referring to numerous biliary, pancreatic, and hepatic disorders resulting from spasms, strictures, and relaxation of this valve at inappropriate times. This review brings attention to various factors that may increase the risk of SOD, including but not limited to: cholecystectomy, opiates, and alcohol. Lack of proper recognition and treatment of SOD may be associated with clinical events, including pancreatitis and biliary symptoms with hepatic enzyme elevation. Pharmacologic and non-pharmacologic approaches are discussed to help recognize, prevent, and treat SOD. Future studies are needed to assess the treatment benefit of agents such as calcium-channel blockers, glyceryl trinitrate, or tricyclic antidepressants in patients with SOD.

У дослідженні були вивчені особливості змін факторів агресії та захисту у вмісті шлункового соку в 91 пацiєнта iз гастроезофагеальною рефлюксною хворобою (ГЕРХ) у поєднанні з дисфункцією сфінктера Одді. Визначали рН, концентрацію пепсину, глікопротеїнів, жовчних кислот, сіалових кислот, фукози, гексозамінів, рівень метаболітів оксиду азоту. Встановлено, що підвищення рівня метаболітів оксиду азоту та жовчних кислот у шлунковому соку призводить до посилення запальних процесів у слизовій оболонці шлунка незалежно від функціонального стану сфінктера Одді. Збільшення агресивних властивостей шлункового вмісту спостерігалось у пацієнтів із ГЕРХ як із гіпертонусом, так і гіпотонусом сфінктера Одді. Дефіцит та диспропорція факторів захисту в більшості хворих в усіх групах проявлялись у вигляді зменшення концентрації вуглеводних термінальних залишків глікопротеїнів відносно показників контрольної групи., В исследовании были изучены особенности изменений факторов агрессии и защиты в желудочном соке у 91 пациента с гастроэзофагеальной рефлюксной болезнью (ГЭРБ) в сочетании с дисфункцией сфинктера Одди. Определяли рН, концентрацию пепсина, гликопротеинов, желчных кислот, сиаловых кислот, фукозы, гексозаминов, уровень метаболитов оксида азота. Установлено, что повышение уровня метаболитов оксида азота и желчных кислот в желудочном соке приводит к усилению воспалительных процессов в слизистой оболочке желудка независимо от функционального состояния сфинктера Одди. Увеличение агрессивных свойств желудочного содержимого наблюдалось у пациентов с ГЭРБ как с гипертонусом, так и гипотонусом сфинктера Одди. Дефицит и диспропорция факторов защиты у большинства пациентов во всех группах проявлялись в виде уменьшения концентрации углеводных терминальных остатков гликопротеинов относительно показателей контрольной группы., There were studied the features of changes in the factors of aggression and protection in the gastric juice of 91 patients with gastroesophageal reflux disease (GERD) combined with sphincter of Oddi dysfunction. It was determined the pH, concentration of pepsin, glycoproteins, bile acids, sialic acids, fucose, hexosamines, the level of nitric oxide metabolites. It has been found that increased levels of nitric oxide metabolites and bile acids in gastric juice enhances the inflammatory processes in the gastric mucosa irrespective of the functional state of the sphincter of Oddi. Aggressive properties of gastric contents were increased in patients with GERD associated with both hypertonic and hypotonic sphincter of Oddi. The deficit and imbalance of protection factors in most patients in all groups were manifested by reduction in the concentration of carbohydrate terminal residues of glycoproteins as compared to the control group.

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 greater than or equal to 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.

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 greater than or equal to 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.