Altered sphincter of Oddi Phasic Activity following truncal vagotomy

Neural as well as hormonal influences regulate sphincter of Oddi function. Therefore, we tested the hypothesis that truncal vagotomy alters sphincter of Oddi phasic activity and response to hormonal stimulation. Adult, male prairie dogs underwent either sham laparotomy or truncal vagotomy and pyloroplasty. Postoperatively, all animals were fed a trace-cholesterol (nonlithogenic) diet for 3 months. In acute terminal experiments the distal common bile duct was perfused with lactated Ringer's solution at 0.1 ml/min. Sphincter of Oddi (SO) phasic contractions as well as baseline resistance were recorded before and during a 30-minute intravenous infusion of 10 ng/kg/min of cholecystokinin-octapeptide (CCK-OP). Before the CCK-OP infusion, both the frequency and amplitude of SO phasic contractions were significantly greater (P < 0.01) in vagotomized animals. During CCK-OP, the frequency of SO phasic contractions remained significantly greater (P < 0.01) in the vagotomy animals. The amplitude of SO phasic contractions, however, increased significantly (P < 0.03) in response to CCK-OP only in sham animals. Vagotomized animals failed to develop any further increase in the amplitude of SO phasic contractions during CCK-OP infusion. No differences in baseline resistance were noticed between sham and vagotomized animals before or during the infusion of CCK-OP. These findings suggest that (1) vagal tone inhibits sphincter of Oddi phasic contractions, (2) vagotomy increases sphincter of Oddi phasic activity, and (3) parasympathetic denervation alters the sphincter of Oddi's response to CCK-OP. Since the sphincter of Oddi plays an important role in normal gallbladder filling and emptying, altered sphincter of Oddi function may, in part, be responsible for the gallbladder stasis observed following vagotomy.     

Duodenal acidification inhibits sphincter of Oddi motility in the prairie dog

Recent studies have explored the influence of various hormones, peptides, and neural innervation on the sphincter of Oddi (SO). However, only older and conflicting data are available on the effect of intraduodenal (ID) perfusion of acid on SO activity. Therefore, we tested the hypothesis that acidification of the proximal small bowel would alter SO motility. In acute terminal experiments, 19 adult male prairie dogs underwent cannulation of the gallbladder (GB) with a pressure-monitored perfusion catheter. The common bile duct was cannulated proximally with a drainage catheter and distally with a triple-lumen, side-hole, closed-tip catheter with one port positioned in the SO. The duodenum was cannulated distal to the SO to allow perfusion of the proximal 30 cm of intestine with saline. SO phasic wave frequency (F), amplitude (A), and baseline pressure as well as GB pressure were measured for 40 min prior to and during ID perfusion of saline at pH 8.8, pH 6.0, or pH 2.0. A SO motility index (MI = F X A) was calculated for each 10-min period of the experiment. Infusion of saline at pH 8.8 had no effect on SO function. ID perfusion of saline at pH 6.0 reduced SO MI to 39% (P less than 0.05) and 34% (P less than 0.05) of control values at 20-30 and 30-40 min, respectively. ID saline at pH 2.0 reduced the SO MI to 51% (P less than 0.01) and 53% of control values during the same periods.(ABSTRACT TRUNCATED AT 250 WORDS)     

Neuropeptide Y: a candidate neurotransmitter for biliary motility

Neuropeptide Y (NPY) is a recently discovered polypeptide found in neurons throughout the gastrointestinal tract and in especially high concentrations in the biliary tree. This study was designed to test the functional significance of these high concentrations in the biliary tree by determining the effect of intravenous NPY on sphincter of Oddi and gallbladder motility. In adult male prairie dogs a side-hole, pressure-monitored perfusion catheter was placed through a choledochotomy into the duodenum and positioned in the sphincter of Oddi. A perfusion catheter was also placed in the gallbladder fundus. Sphincter of Oddi and gallbladder pressures were recorded before and during intravenous infusions of NPY at doses of 10, 100, and 500 ng/kg/min. Each dose was administered to seven separate animals. No effects were seen at the 10 or 100 ng/kg/min doses. NPY at the 500 ng/kg/min dose significantly increased sphincter of Oddi phasic wave frequency, amplitude, and motility index (MI = F X A). In addition, gallbladder pressure was significantly increased after 20 min of intravenous infusion of NPY at the 500 ng/kg/min dose. No significant changes in blood pressure were noted. These data suggest that in the prairie dog, systemic intravenous infusion of NPY significantly increases sphincter of Oddi phasic wave activity and gallbladder pressure. These findings are similar to those observed with intravenous cholecystokinin but opposite of those seen with peptide YY in this species. We hypothesize that neuropeptide Y may be an important neurotransmitter or neuromodulator regulating bile flow.     

Peptide YY inhibits cholecystokinin-stimulated sphincter of Oddi activity in the prairie dog

Peptide YY (PYY), a recently discovered gut peptide, has been shown to have a number of actions that are antagonistic to the effects of cholecystokinin. This study was designed to determine whether PYY would inhibit cholecystokinin-stimulated sphincter of Oddi activity in the prairie dog. In 12 prairie dogs PYY was infused intravenously at 1, 10, and 100 ng/kg/min, and arterial blood samples were obtained. A dose-response curve was obtained, with the 10 ng/kg/min dose producing serum levels of 725 pg/ml. In seven additional prairie dogs a side-hole, pressure-monitored perfusion catheter was passed into the duodenum through a choledochotomy and positioned in the sphincter of Oddi. A perfusion catheter was also placed in the gallbladder fundus. Sphincter of Oddi and gallbladder pressures were recorded before and during 20-minute infusions of cholecystokinin and then cholecystokinin plus PYY at 10 ng/kg/min. PYY significantly inhibited cholecystokinin-stimulated sphincter of Oddi phasic wave frequency (3.8 +/- 0.2 vs 3.3 +/- 0.4; p less than 0.05) and sphincter of Oddi motility index (26.2 +/- 4.3 vs 18.7 +/- 4.8; p less than 0.025) but did not affect the increase in gallbladder pressure induced by cholecystokinin. These findings are consistent with other known anticholecystokinin effects of PYY. We conclude that PYY may also inhibit sphincter of Oddi activity in the prairie dog by an anticholecystokinin effect, thus reducing flow through the sphincter.     

Cholecysto-Sphincter Inhibitory Reflex: Identification of a Reflex and Its Role in Bile Flow in a Canine Model

To study the effect of gallbladder (GB) distension on the sphincter of Oddi (SO), 9 mongrel dogs (mean weight 15.3 ± 3.6 kg) were studied. Under anesthesia, the abdomen was opened and the GB and SO were exposed. A balloon-tipped catheter was introduced into the GB and a manometric catheter into the common bile duct so that its fluoroscopically controlled tip lay within the SO. The pressure response of the GB and SO to GB distension by the balloon without and with selective anesthetization of the GB and SO was recorded. The test was repeated in four vagotomized dogs. GB distension effected pressure rise within the GB and pressure drop within the SO. The GB pressure increased progressively as the distending volume increased, while the SO pressure drop was not affected. Selective anesthetization of the GB or the SO produced no SO pressure changes upon GB distension. The SO pressure response to GB distension after vagotomy was similar to that before vagotomy. The SO relaxation on GB contraction, being reproducible and abolished by selective anesthetization of either the SO or the GB, postulates a reflex relationship that we call the cholecysto-sphincter inhibitory reflex. This reflex seems to regulate the bile flow from the GB to the duodenum through the SO.     

Cholecystectomy alters the hormonal response of the sphincter of Oddi

We have previously described a cholecysto-sphincter of Oddi reflex whereby sphincter of Oddi (SO) motility is mediated in part by the degree of gallbladder distension. Therefore, we tested the hypothesis that cholecystectomy alters the response of the SO to endogenous and exogenous hormonal stimulation. Eight months after sham laparotomy (n = 8) or cholecystectomy (n = 10), prairie dogs were anesthetized with alpha-chloralose. The common bile duct was cannulated distally with a side-hole, pressure-monitored catheter perfused with degassed water at 0.15 ml/min. The duodenum was cannulated distal to the SO to allow perfusion of the proximal 30 cm of intestine with 20 mmol/L sodium oleate at 0.4 ml/min. In animals undergoing sham laparotomy the gallbladder was cannulated, aspirated, and kept empty throughout the experiment. SO phasic wave frequency (F), amplitude (A), and baseline pressure were measured for 60 minutes before and during intraduodenal (ID) perfusion of sodium oleate and then for 60 minutes before and 30 minutes during intravenous (IV) infusion of cholecystokinin-octapeptide (CCK-OP) at 10 ng/kg/min. A SO motility index (MI) (MI = F X A) was calculated for each 10-minute period. Common duct diameter and resting SO motility were unaltered 8 months after cholecystectomy. In animals that had sham laparotomy ID infusion of sodium oleate reduced SO MI by 46% (p = 0.06) and 75% (p less than 0.05) at 30 and 60 minutes, respectively, whereas in animals that had cholecystectomy the reduction in SO MI was only 6% and 25% (p less than 0.05) during the same periods. In animals that had sham laparotomy IV CCK-OP increased the SO MI by 175% (p less than 0.05), but in the animals that had cholecystectomy IV CCK-OP increased SO MI by only 60% (no significance). These findings indicate that after cholecystectomy resting SO motility is unaltered, but the response to ID sodium oleate and to IV cholecystokinin is blunted. We suggest that cholecystectomy alters neural pathways that mediate the normal response of the SO to endogenous and exogenous hormonal stimulation.     

犬胆囊、Oddi括约肌电活动和胆囊胆总管压力的同步检测

目的探讨同步检测犬胆囊、Oddi括约肌肌电和胆囊、胆总管压力的实验方法。方法采用多通道生理仪同步记录麻醉后犬的胆囊和Oddi括约肌的肌电图以及胆囊、胆总管压力。剖腹显示肝、胆、胃及十二指肠,用7F静脉深穿管经肝穿刺进入胆囊腔内作为测压通道,再将一对铂金电极缝在胆囊底部浆膜上。把另一条7F静脉深穿管制作成带一对铂金电极的胆总管测压和Oddi括约肌肌电检测通道。结果Oddi括约肌峰电位为0．18～0．20mV,频率为2～5次／min;其慢波电位0．06～0．08mV,频率为8～10次／min,峰电位往往在某次慢波电位的基础上突然出现。胆囊肌电不明显。胆囊的压力为7～9cmH2O,胆总管压力为11～15cmH2O。结论同步检测Oddi括约肌肌电活动与胆囊、胆总管压力的实验方法是可行的,有利于研究Oddi括约肌肌电活动与胆囊及胆总管压力的关系,但是对于记录在体胆囊的肌电活动方法需要进一步改进。     

Sphincter of Oddi motility disorders in patients with idiopathic recurrent pancreatitis

Motor disorders of the sphincter of Oddi (SO) may play a role in the pathogenesis of idiopathic recurrent pancreatitis. We have compared manometric records from the SO in 28 patients with idiopathic recurrent pancreatitis with those from 10 control subjects. Patients with idiopathic recurrent pancreatitis had presented with episodes of upper abdominal pain associated with abnormal serum levels of amylase on at least two occasions, in the absence of alcohol abuse and biliary disease. Retrograde pancreatography was either normal or showed only minor changes in pancreatic ducts. A triple lumen low compliance manometric system was used to obtain a 5 min recording of spontaneous SO motor activity. From this recording were determined the SO basal pressure, SO phasic contraction amplitude, SO wave frequency and direction of wave propagation. The SO response to intravenous cholecystokinin-octapeptide (CCK-OP) 20 ng/kg was then recorded for at least 3 min. Twenty-five of the twenty-eight patients demonstrated one or more manometric abnormality when compared with data from the ten controls. The most frequent abnormality was an elevated SO basal pressure in 16 patients. In addition, excess of retrograde contractions in nine patients, high frequency of SO phasic contractions in nine patients, absence of phasic contractions in three patients, and paradoxical response to CCK-OP administration in two patients were recorded. This study has demonstrated a spectrum of sphincter of Oddi manometric disorders in patients with idiopathic recurrent pancreatitis and suggests that motility disorders of the sphincter of Oddi may be associated with episodes of pancreatitis.     

The role of cystic duct resistance in the pathogenesis of cholesterol gallstones

Several recent clinical and laboratory observations suggest that impaired gallbladder emptying is important in the pathogenesis of cholesterol cholelithiasis. However, the exact mechanism by which gallbladder stasis occurs in the majority of patients who form gallstones has not been clear. We tested the hypothesis that impaired gallbladder emptying antedates cholelithiasis and results from increased resistance to bile flow. Using the prairie dog gallstone model, resistance to flow through the cystic duct (CD) and sphincter of Oddi (SO) was measured in control and cholesterol-fed animals. Prairie dogs were fed either a control (trace cholesterol) or a 0.4% cholesterol-enriched diet known to induce gallstones in 6 weeks. Resistance across the CD and SO was measured at 4 weeks (pregallstone) and 16 weeks (gallstone). Resistance was measured by infusing lactated Ringer's solution through the CD and SO at four separate flow rates while gallbladder and distal common bile duct pressures were recorded. Resistance to flow through the cystic duct increased prior to gallstone formation and continued to increase during the 16 weeks of cholesterol feeding. In comparison, sphincter of Oddi resistance remained normal despite chronic exposure to lithogenic bile and formation of stones within the gallbladder. The increased cystic duct resistance observed prior to gallstone formation provides a mechanism for diminished gallbladder emptying and suggests an etiological role for increased cystic duct resistance in the pathogenesis of cholesterol gallstones.     

Distribution and effect of galanin on gallbladder and sphincter of Oddi motility 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.     

Gastrosphincter of Oddi reflex

Gastric distention is known to stimulate gallbladder contraction as well as gastric acid and pancreatic exocrine secretion by way of neural reflexes. Gallbladder distention, in turn, has been shown to affect sphincter of Oddi motility. Since gastric distention may accompany endoscopic or operative biliary manometry, we tested the hypothesis that gastric distention alters sphincter of Oddi motility. In the prairie dog model, gastric distention with acid (0.1 M hydrochloric acid, pH 1.3) and alkaline (10(-5) sodium hydroxide, pH 8.8) isotonic saline solutions both resulted in significant increases in sphincter of Oddi phasic wave frequency, amplitude, and motility index. Similarly, gallbladder pressure increased during both distention periods, thus confirming the previously described pylorocholecystic reflex. These responses were abolished by systemic pretreatment with atropine, suggesting that this reflex is cholinergically mediated. These data suggest the presence of a gastrosphincter of Oddi reflex whereby gastric distention stimulates sphincter of Oddi motility in the prairie dog. We conclude that gastric distention is an important variable to be controlled when performing endoscopic or operative sphincter of Oddi manometry.     

Human fasting and postprandial sphincter of Oddi motility

Sphincter of Oddi motility was evaluated in post-cholecystectomy patients with indwelling T tubes during fasting and after feeding. A triple-lumen catheter was positioned to record from the sphincter of Oddi and duodenum. The sphincter of Oddi was characterized by phasic contractions independent of duodenal contractions. During fasting duodenal wave frequency exhibited four phases, whereas only two phases could be identified from the sphincter of Oddi. A prolonged phase A in the sphincter of Oddi corresponded to duodenal phases I, II and IV. A short phase B in the sphincter of Oddi just preceded the onset of duodenal phase III and was temporally related to it. Sphincter of Oddi basal pressure increased during duodenal phases III and IV. After ingestion of food, sphincter of Oddi basal pressure, wave amplitude and duration decreased, but the frequency remained unchanged. Conversely, duodenal frequency increased but there was no change in amplitude. Thus, the human sphincter of Oddi and duodenum exhibited independent motility demonstrating distinct phases during the interdigestive period. After food, sphincter of Oddi motility altered in a manner which would facilitate the passive flow of fluid into the duodenum.     

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. Received: March 25, 2002 / Accepted: April 14, 2002 Offprint requests to: M. Tanaka     

生长抑素对Oddi's括约肌功能的影响

目的: 研究生长抑素类似物施他宁对奥狄括约肌(sphincter of Oddi,SO)功能状态的影响.方法: 通过T管窦道经胆道镜途径顺行插入测压管至SO,低压水灌注系统压力传感器与微机相连记录压力曲线,分析软件进行压力曲线分析.结果: 对SO基础压的作用与用药前差异显著(P<0.01);对SO收缩幅度的影响无显著性意义;对SO收缩间期的影响与用药前比较差异显著(P<0.05);对SO收缩频率的影响与用药前比较差异显著(P<0.05).施他宁倍量输入后10 min SO收缩频率与用药前已无差异,与5 μg/min用药10 min比较差异显著(P<0.05).结论: 施他宁显著降低SO基础压,延长收缩间期且具有剂量依赖性.对收缩频率的影响:低剂量时增加,高剂量时抑制;对收缩幅度的作用:高剂量时收缩幅度下降但无显著性意义.     

Inhibition of sphincter of Oddi motility in Australian possum by cholic acid

The effect of intravenous administration of cholic acid on sphincter of Oddi (SO) and gallbladder motility was studied. Bolus doses of cholic acid, 20 to 60 mg/kg, produced inhibition of SO wave frequency, a fall in gallbladder pressure and enhanced bile flow. However, hydrocortisone, 10 and 20 mg/kg, produced comparable elevation in bile flow with no effect on SO and gallbladder motility. The effect of cholic acid on SO motility was not influenced by prior treatment with atropine. Phentolamine or propranolol administration did not influence SO wave frequency SO wave frequency, but subsequent injection of cholic acid resulted in a decrease in SO wave frequency. Gallbladder pressure was not influenced by atropine, phentolamine, or propranolol, and these agents did not influence the cholic acid-induced fall in gallbladder pressure. These findings suggest that bile acids influence the motility of the biliary tract.     

Peroperative sphincter of Oddi manometry: motility disorder in patients with cholelithiasis

Intraluminal pressure recordings from the sphincter of Oddi (SO) have made significant contributions towards the understanding of normal SO function and are being used for the diagnosis of SO motility abnormalities. In this study the endoscopic intraluminal methods for measuring SO pressure changes have been adapted for use under sterile conditions during surgery on the biliary system. Sphincter of Oddi pressure measurement in a group of patients undergoing elective cholecystectomy for gallstones, were compared with a group of control subjects undergoing endoscopic study of the SO. There was no significant difference in CBD pressure. SO basal pressure, SO wave amplitude and SO wave frequency. However, a highly significant difference was noted in the propagation direction of the SO contractions. The control subjects had a predominance of antegrade contractions whereas patients undergoing cholecystectomy had a predominance of retrograde contractions. This result suggests an association between SO motility disorder and the presence of gallstones.     

腹腔镜电针Vater壶腹戳孔导管扩张术和Oddi括约肌切开术的初步探讨

目的 :探讨腹腔镜电针Vater壶腹戳孔导管扩张术和腹腔镜电针Oddi括约肌切开术治疗Oddi括约肌狭窄的手术方法。方法 :采用腹腔镜胆总管探查结合电针 ,套装胆道扩张导管和斑马导丝 ,为 13例胆管结石 ,胆管扩张合并Oddi括约肌狭窄患者行腹腔镜电针Vater壶腹戳孔导管扩张术。结果 :13例手术均获成功 ,无胆漏、出血、穿孔及胰腺炎。结论 :选择合适病例 ,腹腔镜胆总管探查术中采用腹腔镜电针Vater壶腹戳孔导管扩张术和腹腔镜电针Oddi括约肌切开术治疗Oddi括约肌狭窄有效、可行。     

Postprandial sphincter of Oddi myoelectric activity and gallbladder emptying

Feeding initiates gallbladder emptying and bile delivery into the duodenum. It is not yet defined how the sphincter of Oddi regulates flow of bile into the duodenum during gallbladder emptying. The aim of this study was to assess postprandial spike burst activity in the sphincter of Oddi, while quantitating gallbladder emptying with noninvasive radioisotope imaging. Six adult opossums were prepared with bipolar electrodes in the sphincter of Oddi. After 2 weeks of recovery the animals were fasted overnight and positioned under a gamma camera, and myoelectric recordings were begun. After two cycles of the migrating motor complex (MMC), 2 mCi 99Tc-HIDA was infused intravenously and permitted to concentrate in the gallbladder for a period of 30 min. Subsequently, a 30-ml liquid meal, containing 0.9 g protein, 3.5 g carbohydrate, and 3.3 g fat, was instilled into the stomach. Sphincter of Oddi myoelectric activity (spike bursts/min) and gallbladder emptying (expressed as percentage of original 99Tc counts in the gallbladder) were measured at intervals for 120 min following feeding. Feeding resulted in prompt gallbladder emptying. Sphincter of Oddi spike burst activity was not altered significantly in the first 30 min after feeding, suggesting that motor activity in the sphincter of Oddi does not initially influence bile flow. Subsequently, spike burst activity increased progressively, suggesting that sphincter of Oddi motor activity may accelerate bile delivery into the duodenum during later phases of gallbladder emptying.     

A comparison of common bile duct pressures after botulinum toxin injection into the sphincter of Oddi versus biliary stenting in a canine model

BACKGROUND: Botulinum toxin A (Botox) functionally paralyzes the sphincter of Oddi in both animals and humans, resulting in reduced pressures. No study, however, has specifically addressed common bile duct (CBD) pressures after Botox injection into the sphincter of Oddi with regard to treating biliary leaks and fistulae. The goals of this present study are to compare, versus biliary stenting, the change in CBD pressures after Botox injection into the sphincter of Oddi, as well as to evaluate the timing of onset and duration of these effects on sphincteric relaxation. METHODS: After midline laparotomy in 20 mongrel dogs, a pediatric umbilical catheter was inserted into the CBD via a small cholecystotomy and attached to a water-perfused pressure transducer. After baseline CBD pressure readings, a lateral duodenotomy was performed. A total of 100 units of Botox was injected with an endoscopic sclerotherapy needle into all four quadrants of the ampulla. The dogs were randomly divided into four groups to undergo repeat laparotomy at either postoperative day 1 (group I), postoperative day 3 (group II), postoperative day 7 (group III), or postoperative day 14 (group IV). At the time of second laparotomy, a pressure-sensing catheter was reinserted into the CBD and pressures recorded. Each dog then underwent transpapillary biliary stenting with a 7 Fr. x 5 cm Cotton-Leung biliary stent and CBD pressures were again recorded. RESULTS: CBD pressures were significantly lower as compared with baseline for all groups after Botox injection and after biliary stenting (P <0.001) In addition, no significant differences in the degree of CBD pressure reduction were identified between groups I through IV after Botox injection. The measured decrease in CBD pressure from baseline after Botox injection as compared with biliary stenting was significantly different for groups I and II (P <0.05) but not for groups III and IV. CONCLUSION: Botox injection into the sphincter of Oddi results in significant CBD pressure reduction within 24 hours and continues for 14 days. Also, after postoperative day 3, there is no significant difference in the reduction of CBD pressure from baseline between Botox injection and biliary stenting. Based on these findings, Botox injection into the sphincter of Oddi may be a beneficial alternative to biliary stenting for the treatment of biliary leaks and fistulae.     

Ethanol inhibits sphincter of oddi motility

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. Supported by National Institutes of Health grants R29-DK41889 (K.D.L.) and R01-DK44279 (H.A.P.)