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Keith D. Lillemoe - One of the best experts on this subject based on the ideXlab platform.

  • Effect of octreotide on Sphincter of Oddi and gallbladder motility in prairie dogs
    2016
    Co-Authors: Steven A. Ahrendt, Keith D. Lillemoe, Gretchen M. Ahrendt, A. Pitt, Steven A, Keith D
    Abstract:

    ter of Oddi and gallbladder motility in prairie dogs. Am. J. Physiol. 262 (Gastrointest. Liver Physiol. 25): G909-G914, 1992.-Somatostatin and its synthetic analogue, octreotide, inhibit gallbladder emptying and cause gallstones. Whether oct-reotide-induced alterations in Sphincter of Oddi motility con-tribute 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 oct-reotide decreased fasting Sphincter of Oddi motility index bot

  • Ethanol inhibits Sphincter of Oddi motility
    Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 1998
    Co-Authors: Sean Tierney, Zhiping Qian, Pamela A. Lipsett, Henry A. Pitt, Keith D. Lillemoe
    Abstract:

    Patients with alcohol-induced liver disease are at increased risk for pigment gallstones, which are known to be particularly associated with biliary stasis. Although the effects of ethanol on the Sphincter of Oddi are thought to contribute to alcoholic pancreatitis, the precise effects of ethanol on the biliary component of the Sphincter of Oddi are unclear. In the prairie dog the common bile and pancreatic ducts enter the duodenum separately, facilitating pressure measurement in the Sphincter choledochus in isolation. We therefore used this model to test the hypothesis that ethanol administration alters Sphincter of Oddi motility. Twenty-six male prairie dogs fed a nonlithogenic diet were studied. With the animals under α-chloralose anesthesia, a side-hole pressure-monitored perfusion catheter was positioned in the Sphincter of Oddi and femoral arterial and venous catheters were placed. Sphincter of Oddi phasic wave frequency (F), amplitude (A), and motility index (MI = F × A) and arterial blood pressure were monitored at 10-minute intervals before (baseline), during 20-minute intravenous infusions of 15 mg/kg (n = 9), 150 mg/kg (n = 10), and 1.5 g/kg (n = 7) ethanol and for 20 minutes after ethanol infusion. The 15 mg/kg dose of ethanol had no effect, the 150 mg/kg dose tended to reduce Sphincter of Oddi motility, and significant reductions in Sphincter of Oddi amplitude and motility index were seen at the 1.5 g/kg dose. These data demonstrate that ethanol infusion inhibits both Sphincter of Oddi amplitude and motility index and that this effect persists for at least 20 minutes following ethanol infusion. Ethanol may contribute to gallstone formation by altering biliary Sphincter motility.

  • Gender influences Sphincter of Oddi response to cholecystokinin in the prairie dog.
    The American journal of physiology, 1995
    Co-Authors: S Tierney, H A Pitt, Z Qian, B Yung, P A Lipsett, S Sostre, Keith D. Lillemoe
    Abstract:

    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.

  • Estrogen inhibits Sphincter of Oddi motility.
    The Journal of surgical research, 1994
    Co-Authors: Sean Tierney, Zhiping Qian, Pamela A. Lipsett, Henry A. Pitt, C. Burrow, Keith D. Lillemoe
    Abstract:

    Gallstones and Sphincter of Oddi dysfunction are both more common in women than men, suggesting that endogenous hormones may play an important role in these conditions. Female sex hormones are known to affect cholesterol metabolism and gallbladder motility. However, the effect of these hormones on the Sphincter of Oddi has not previously been studied. We therefore tested the hypothesis that exogenous estrogen administration would inhibit Sphincter of Oddi motility. Twenty-three male prairie dogs fed a nonlithogenic diet were studied. Under alpha-chloralose anesthesia, a side hole pressure-monitored perfusion catheter was positioned in the Sphincter of Oddi and perfused with degassed water at 0.15 ml/min. Femoral arterial and venous catheters were placed. Sphincter of Oddi phasic wave frequency (F), amplitude (A), and motility index (MI = F x A), as well as arterial blood pressure (BP), were monitored for 10-min intervals before (control), during 20-min intravenous infusions of 0.1, 1, or 10 micrograms/kg beta-estradiol, and for 20 min after estradiol infusion. No response was observed at the 0.1- or 1-micrograms doses. Sphincter of Oddi motility was significantly (P < 0.05) reduced during estrogen infusion at the higher dose of 10 micrograms, primarily due to decreased phasic wave frequency. Sphincter motility remained depressed for at least 20 min following estrogen infusion. We conclude that estrogen effects on the Sphincter of Oddi may contribute to the higher incidence of gallstones and Sphincter dysfunction seen in premenopausal women.

  • Nitric oxide inhibits resting Sphincter of Oddi activity
    American journal of surgery, 1993
    Co-Authors: Howard S. Kaufman, Henry A. Pitt, Michele A. Shermak, Christopher A. May, Keith D. Lillemoe
    Abstract:

    The Sphincter of Oddi has basal myogenic phasic activity that is modulated by neural and hormonal pathways. Stimulatory innervation to this organ is cholinergic, whereas the inhibitory pathways are unknown. Nitric oxide (NO), generated from L-arginine, relaxes gastrointestinal smooth muscle in vitro. We, therefore, hypothesized that resting Sphincter of Oddi and duodenal motilities are regulated by a NO-mediated inhibitory pathway. In 23 anesthetized prairie dogs, systemic blood pressure and Sphincter of Oddi and duodenal motilities were monitored during systemic infusion of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase. L-NAME was infused alone and simultaneously with excess D- and L-arginine. L-NAME alone and L-NAME with D-arginine produced hypertension and increased Sphincter of Oddi and duodenal motilities. L-arginine blocked these increases, suggesting that baseline Sphincter of Oddi and duodenal motility regulation involves the generation of NO from L-arginine. We conclude that baseline Sphincter of Oddi phasic activity is regulated by cholinergic stimulatory and NO-mediated inhibitory neural pathways.

Henry A. Pitt - One of the best experts on this subject based on the ideXlab platform.

  • Ethanol inhibits Sphincter of Oddi motility
    Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 1998
    Co-Authors: Sean Tierney, Zhiping Qian, Pamela A. Lipsett, Henry A. Pitt, Keith D. Lillemoe
    Abstract:

    Patients with alcohol-induced liver disease are at increased risk for pigment gallstones, which are known to be particularly associated with biliary stasis. Although the effects of ethanol on the Sphincter of Oddi are thought to contribute to alcoholic pancreatitis, the precise effects of ethanol on the biliary component of the Sphincter of Oddi are unclear. In the prairie dog the common bile and pancreatic ducts enter the duodenum separately, facilitating pressure measurement in the Sphincter choledochus in isolation. We therefore used this model to test the hypothesis that ethanol administration alters Sphincter of Oddi motility. Twenty-six male prairie dogs fed a nonlithogenic diet were studied. With the animals under α-chloralose anesthesia, a side-hole pressure-monitored perfusion catheter was positioned in the Sphincter of Oddi and femoral arterial and venous catheters were placed. Sphincter of Oddi phasic wave frequency (F), amplitude (A), and motility index (MI = F × A) and arterial blood pressure were monitored at 10-minute intervals before (baseline), during 20-minute intravenous infusions of 15 mg/kg (n = 9), 150 mg/kg (n = 10), and 1.5 g/kg (n = 7) ethanol and for 20 minutes after ethanol infusion. The 15 mg/kg dose of ethanol had no effect, the 150 mg/kg dose tended to reduce Sphincter of Oddi motility, and significant reductions in Sphincter of Oddi amplitude and motility index were seen at the 1.5 g/kg dose. These data demonstrate that ethanol infusion inhibits both Sphincter of Oddi amplitude and motility index and that this effect persists for at least 20 minutes following ethanol infusion. Ethanol may contribute to gallstone formation by altering biliary Sphincter motility.

  • Estrogen inhibits Sphincter of Oddi motility.
    The Journal of surgical research, 1994
    Co-Authors: Sean Tierney, Zhiping Qian, Pamela A. Lipsett, Henry A. Pitt, C. Burrow, Keith D. Lillemoe
    Abstract:

    Gallstones and Sphincter of Oddi dysfunction are both more common in women than men, suggesting that endogenous hormones may play an important role in these conditions. Female sex hormones are known to affect cholesterol metabolism and gallbladder motility. However, the effect of these hormones on the Sphincter of Oddi has not previously been studied. We therefore tested the hypothesis that exogenous estrogen administration would inhibit Sphincter of Oddi motility. Twenty-three male prairie dogs fed a nonlithogenic diet were studied. Under alpha-chloralose anesthesia, a side hole pressure-monitored perfusion catheter was positioned in the Sphincter of Oddi and perfused with degassed water at 0.15 ml/min. Femoral arterial and venous catheters were placed. Sphincter of Oddi phasic wave frequency (F), amplitude (A), and motility index (MI = F x A), as well as arterial blood pressure (BP), were monitored for 10-min intervals before (control), during 20-min intravenous infusions of 0.1, 1, or 10 micrograms/kg beta-estradiol, and for 20 min after estradiol infusion. No response was observed at the 0.1- or 1-micrograms doses. Sphincter of Oddi motility was significantly (P < 0.05) reduced during estrogen infusion at the higher dose of 10 micrograms, primarily due to decreased phasic wave frequency. Sphincter motility remained depressed for at least 20 min following estrogen infusion. We conclude that estrogen effects on the Sphincter of Oddi may contribute to the higher incidence of gallstones and Sphincter dysfunction seen in premenopausal women.

  • Nitric oxide inhibits resting Sphincter of Oddi activity
    American journal of surgery, 1993
    Co-Authors: Howard S. Kaufman, Henry A. Pitt, Michele A. Shermak, Christopher A. May, Keith D. Lillemoe
    Abstract:

    The Sphincter of Oddi has basal myogenic phasic activity that is modulated by neural and hormonal pathways. Stimulatory innervation to this organ is cholinergic, whereas the inhibitory pathways are unknown. Nitric oxide (NO), generated from L-arginine, relaxes gastrointestinal smooth muscle in vitro. We, therefore, hypothesized that resting Sphincter of Oddi and duodenal motilities are regulated by a NO-mediated inhibitory pathway. In 23 anesthetized prairie dogs, systemic blood pressure and Sphincter of Oddi and duodenal motilities were monitored during systemic infusion of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase. L-NAME was infused alone and simultaneously with excess D- and L-arginine. L-NAME alone and L-NAME with D-arginine produced hypertension and increased Sphincter of Oddi and duodenal motilities. L-arginine blocked these increases, suggesting that baseline Sphincter of Oddi and duodenal motility regulation involves the generation of NO from L-arginine. We conclude that baseline Sphincter of Oddi phasic activity is regulated by cholinergic stimulatory and NO-mediated inhibitory neural pathways.

  • effect of octreotide on Sphincter of Oddi and gallbladder motility in prairie dogs
    American Journal of Physiology-gastrointestinal and Liver Physiology, 1992
    Co-Authors: Steven A. Ahrendt, Keith D. Lillemoe, Gretchen M. Ahrendt, Henry A. Pitt
    Abstract:

    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.

Jeffrey L. Conklin - One of the best experts on this subject based on the ideXlab platform.

  • The effect of peroxynitrite on Sphincter of Oddi motility.
    The Journal of surgical research, 1999
    Co-Authors: Brian W. Herrmann, Joseph J. Cullen, Amber Ledlow, Joseph A. Murray, Jeffrey L. Conklin
    Abstract:

    Background. Nitric oxide (NO . ) is an inhibitory neurotransmitter that induces Sphincter of Oddi relaxation. Superoxide (O 2 .- )-scavenging enzymes are present in enteric plexuses of the Sphincter of Oddi and O 2 .- alters Sphincter of Oddi motor function. O 2 .- rapidly oxidizes nitric oxide (NO . ) to form peroxynitrite (ONOO - ), thus terminating the biological activity of NO . . The aim of our study was to determine the effects of ONOO - on Sphincter of Oddi motility in vitro. Materials and methods. Adult opossums were sacrificed and the Sphincter of Oddi was removed and placed in a tissue bath containing oxygenated Krebs solution at 37°C. In the first series of experiments, force transducers recorded tension in a transverse orientation at two sites along the spontaneously contracting Sphincter of Oddi. In a second series of experiments, circular muscle strips were precontracted with carbachol and stimulated by an electrical field. Results. ONOO - , superoxide dismutase (SOD), N ω -nitro-L-arginine (L-NNA), or oxyhemoglobin were added to the tissue baths. ONOO - decreased the frequency of contractions in the spontaneously contracting Sphincter of Oddi. Adding hemoglobin increased the frequency of contractions. ONOO - also increased the stimulation-induced relaxation compared to controls. The increase in relaxation induced by ONOO - was inhibited by oxyhemoglobin and L-NNA but not SOD. Pretreatment with oxyhemoglobin prevented the increase in the stimulation-induced relaxation caused by ONOO - . Conclusion. These results suggest that hemoglobin binds ONOO - or that ONOO - generates NO.

  • The role of antioxidant enzymes in the control of opossum Sphincter of Oddi motility
    American Journal of Physiology-Gastrointestinal and Liver Physiology, 1997
    Co-Authors: Joseph J. Cullen, Amber Ledlow, Joseph A. Murray, Brian M. Herrmann, R. M. Thomas, Shengyun Fang, James G. Christensen, Jeffrey L. Conklin
    Abstract:

    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.

  • Effect of Hydroxyl Radical (OH•) on Sphincter of Oddi Motility
    Digestion, 1997
    Co-Authors: Joseph J. Cullen, Amber Ledlow, Joseph A. Murray, Jeffrey L. Conklin
    Abstract:

    Antioxidant enzymes are present in Sphincter of Oddi nerves and regulate Sphincter of Oddi motor function mediated by NO-releasing nerves. Oxygen free radicals (O-2) produce hydr

  • The Effect of Ethanol on Sphincter of Oddi Motilityin Vitro
    The Journal of surgical research, 1997
    Co-Authors: Joseph J. Cullen, Amber Ledlow, Joseph A. Murray, Jeffrey L. Conklin
    Abstract:

    Abstract Antioxidant enzymes are present in nerves supplying the Sphincter of Oddi and regulate its motor function. Oxygen free radicals (O 2 •− ) produce hydrogen peroxide (H 2 O 2 ) by the action of superoxide dismutase (SOD). Hydroxyl radical (OH • ), an important mediator of H 2 O 2 toxicity, oxidizes ETOH. Thus, the aim of our study was determine the effects of ETOH on Sphincter of Oddi motility. The Sphincter of Oddi was removed from opossums and force transducers recorded tension in its transverse axis. Alcohol (ETOH) was added to the tissue bath in concentrations from 0.1 to 0.4%. OH • was generated by the addition of 0.01% H 2 O 2 . Nitric oxide production was inhibited by the addition of 0.3 m M N ω -nitro- l -arginine ( l -NNA). H 2 O 2 increased the frequency of Sphincter of Oddi contractions. Concentrations of ETOH >0.3% decreased contractile frequency; however, 0.2% ETOH alone had no affect on the basal frequency of contraction but inhibited the increase in contractile frequency caused by H 2 O 2 . l -NNA also increased the contractile frequency; however, this effect was not inhibited by ETOH. We conclude that ETOH attenuates the effect of H 2 O 2 on Sphincter of Oddi motility.

Stuart Sherman - One of the best experts on this subject based on the ideXlab platform.

  • Is Repeat Sphincter of Oddi Manometry Needed in Symptomatic Patients
    NEJM Journal Watch, 2004
    Co-Authors: Stuart Sherman
    Abstract:

    Sphincter of Oddi manometry (SOM) is considered to be the gold standard for evaluating patients with suspected Sphincter of Oddi dysfunction (SOD). SOM typically is performed at ERCP during a 3- to 10-minute period. Thus, SOM might not document an intermittent motor disorder. Researchers in South Carolina examined the frequency …

  • frequency of biliary crystals in patients with suspected Sphincter of Oddi dysfunction
    Gastrointestinal Endoscopy, 2003
    Co-Authors: Abdullah Rashdan, Lee Mchenry, Evan L Fogel, Glen A Lehman, Stuart Sherman
    Abstract:

    Abstract Background The passage of gallstones (macro- or microlithiasis) is theorized to play a role in inducing Sphincter of Oddi dysfunction. This study examined the frequency at which biliary crystals are found in patients with suspected type II and type III Sphincter of Oddi dysfunction. Methods A total of 85 patients (66 women, 19 men; mean age 38 years) with unexplained abdominal pain of suspected pancreatobiliary origin and no prior episode of pancreatitis underwent ERCP with Sphincter of Oddi manometry and bile collection for crystal analysis. Eighty-one patients had a gallbladder in situ. No patient had evidence of stones or sludge on prior abdominal imaging. Sphincter of Oddi manometry was performed in standard retrograde fashion by using an aspirating catheter. Patients were classified by Sphincter of Oddi dysfunction type by using a modified Hogan-Geenen classification system. Patients with type I Sphincter of Oddi dysfunction were excluded. Bile was collected directly from the gallbladder (n=23) or common bile duct (n=62) after an infusion of 3.5 μg of cholecystokinin and was examined by light and polarizing microscopy for cholesterol crystals or calcium bilirubinate granules. Results The proportion of patients with crystals was 3.5% (3/85). Thirty-five patients (41%) had elevated biliary and/or pancreatic Sphincter pressure (type II, 16; type III, 19), of whom one (3%) had cholesterol crystals. Fifty patients had normal Sphincter pressure, of whom two (4%) had cholesterol crystals ( p =0.6). All 3 patients with cholesterol crystals had a gallbladder in situ. Calcium bilirubinate granules were not found in any patient. Conclusions Microlithiasis appears to be rare in patients suspected to have type II or type III Sphincter of Oddi dysfunction. Evaluation of bile for crystals appears unproductive in this group of patients.

  • Biliary Scintigraphy Correlates Poorly with Sphincter of Oddi Manometry
    NEJM Journal Watch, 2003
    Co-Authors: Stuart Sherman
    Abstract:

    Sphincter of Oddi manometry (SOM) is the gold standard for assessing Sphincter of Oddi dysfunction (SOD). However, SOM is technically difficult to

  • Prevalence of Sphincter of Oddi Dysfunction
    NEJM Journal Watch, 2003
    Co-Authors: Stuart Sherman
    Abstract:

    Sphincter of Oddi manometry is the gold standard for diagnosing Sphincter of Oddi dysfunction (SOD). Investigators in Alabama assessed the prevalence of manometrically documented SOD in 51 patients with unexplained abdominal pain (35 patients), acute recurrent pancreatitis (12), chronic pancreatitis (3), or acute pancreatitis (1). Before manometry, patients were classified as having biliary or pancreatic SOD using the modified Milwaukee classification system on the basis of the clinical …

  • Pancreatitis After Sphincter of Oddi Manometry
    NEJM Journal Watch, 2003
    Co-Authors: Stuart Sherman
    Abstract:

    Pancreatitis is the most common complication of Sphincter of Oddi manometry (SOM). To determine whether microtransducer manometry (MTM) reduces the risk, German researchers prospectively evaluated the frequency of pancreatitis after MTM in 215 consecutive patients and then randomly assigned the 130 patients with clinical suspicion of biliary or pancreatic Sphincter of Oddi dysfunction (SOD) to undergo MTM or standard …

James Toouli - One of the best experts on this subject based on the ideXlab platform.

  • Sphincter of Oddi function dysfunction and its management
    Journal of Gastroenterology and Hepatology, 2009
    Co-Authors: James Toouli
    Abstract:

    The most common functional disorder of the biliary tract and pancreas relates to the activity of the Sphincter of Oddi. The Sphincter of Oddi is a small smooth muscle Sphincter strategically placed at the junction of the bile duct, pancreatic duct, and duodenum. The Sphincter controls flow of bile and pancreatic juices into the duodenum and prevents reflux of duodenal content into the ducts. Disorder in its motility is called Sphincter of Oddi dysfunction. Clinically this presents either with recurrent abdominal biliary type pain or episodes of recurrent pancreatitis. Manometry may identify the motility abnormalities, the most clinically significant being an abnormally elevated basal pressure. The most effective treatment once an abnormal basal pressure is identified is division of the Sphincter. This is associated with good long-term results.

  • The Sphincter of Oddi and acute pancreatitis--revisited.
    HPB : the official journal of the International Hepato Pancreato Biliary Association, 2003
    Co-Authors: James Toouli
    Abstract:

    Background One of the rare causes of recurrent acute pancreatitis is Sphincter of Oddi dysfunction. This condition is objectively diagnosed by manometry of the Sphincter of Oddi. An abnormally elevated Sphincter of Oddi basal pressure has been shown to predict patients who have a successful outcome after transduodenal Sphincteroplasty and pancreatic duct septoplasty. Methods Forty-nine patients presenting with recurrent pancreatitis and who had manometric stenosis of the Sphincter of Oddi were treated by transduodenal division of the Sphincter of Oddi. Clinical follow-up was conducted over a minimum of 2 years. Results In all, 43 patients were either cured or improved. None of these patients had any further episodes of pancreatitis. Three of these patients developed recurrent symptoms and were noted to have restenosis of the Sphincter of Oddi. They were treated by insertion of an endoscopic stent into the pancreatic duct. Conclusion The results from this series of patients re-affirm the efficacy of transduodenal Sphincteroplasty and septoplasty for treatment of Sphincter of Oddi stenosis in patients presenting with recurrent acute pancreatitis.

  • Sphincter of Oddi dysfunction associated with choledochal cyst
    Journal of Gastroenterology and Hepatology, 2001
    Co-Authors: Alexander G Craig, Longdian Chen, Robert Ta Padbury, Gino T. P. Saccone, John W Chen, James Toouli
    Abstract:

    The pathophysiology of choledochal cysts remains unclear, although an association with anomalous pancreato-biliary junction and the reflux of pancreatic enzymes into the biliary tree is known. Sphincter of Oddi (SO) manometry was performed in three patients with choledochal cysts. All patients exhibited an elevated basal pressure diagnostic of Sphincter of Oddi dysfunction. Two patients exhibited anomalous pancreato-biliary junction. This report suggests an association between the choledochal cyst and Sphincter of Oddi dysfunction, and may suggest that SO dysfunction plays a role in choledochal cyst formation.

  • Sphincter of Oddi dysfunction produces acute pancreatitis in the possum
    Gut, 2000
    Co-Authors: John W Chen, Charmaine Woods, Anthony Thomas, Ann C. Schloithe, James Toouli, Gino T. P. Saccone
    Abstract:

    BACKGROUND Sphincter of Oddi dysfunction has been implicated as a cause of various forms of acute pancreatitis. However, there is no direct evidence to show that Sphincter of Oddi dysfunction can cause obstruction of trans-Sphincteric flow resulting in acute pancreatitis. AIMS To determine if induced Sphincter of Oddi spasm can produce trans-Sphincteric obstruction and, in combination with stimulated pancreatic secretion, induce acute pancreatitis. METHODS In anaesthetised possums, the pancreatic duct was ligated and pancreatic exocrine secretion stimulated by cholecystokinin octapeptide/secretin to induce acute pancreatitis. In separate animals, carbachol was applied topically to the Sphincter of Oddi to cause transient Sphincter obstruction. Sphincter of Oddi motility, trans-Sphincteric flow, pancreatic duct pressure, pancreatic exocrine secretion, plasma amylase levels, and pancreatic tissue damage (histology score) were studied and compared with variables in ligation models. RESULTS Acute pancreatitis developed following stimulation of pancreatic exocrine secretion with peptides after pancreatic duct ligation (p CONCLUSION Induced Sphincter of Oddi dysfunction when coupled with stimulated pancreatic secretion causes acute pancreatitis. This may be an important pathophysiological mechanism causing various forms of acute pancreatitis.

  • Somatostatin stimulates the brush-tailed possum Sphincter of Oddi in vitro and in vivo
    Gastroenterology, 1998
    Co-Authors: Jiaqing Huang, Robert Ta Padbury, Ann C. Schloithe, James Toouli, Robert A. Baker, Michael R. Cox, Maria E. Simula, John R. Harvey, Gino T. P. Saccone
    Abstract:

    Abstract Background & Aims: Somatostatin, a neuropeptide and hormone, is found in the biliary tract of several species. The aim of this study was to map the distribution of somatostatin-like immunoreactive nerve fibers in the extrahepatic biliary tract of the Australian possum and to determine the pharmacological effects of somatostatin 1–14 on Sphincter of Oddi activity in vitro and in vivo. Methods: Tissue was harvested for immunohistochemistry and Sphincter of Oddi for circular or longitudinal muscle contractility. In anesthetized possums, Sphincter of Oddi motility was measured by manometry, and transSphincteric flow was measured gravimetrically. Results: Somatostatin immunoreactivity was evident in gallbladder ganglia nerve cell bodies and in nerve fibers of the common bile duct and Sphincter of Oddi. Somatostatin 1–14 increased circular and longitudinal muscle contraction amplitude 3–4-fold ( P P P Conclusions: Somatostatin-like immunoreactivity is present in the extrahepatic biliary tree, and somatostatin 1–14 stimulates Sphincter of Oddi smooth muscle and nerves. The major action is direct stimulation of Sphincter of Oddi circular muscle, which reduces transSphincteric flow. GASTROENTEROLOGY 1998;115:672-679