同步检测胆囊及Oddi氏括约肌电活动和胆管压力的兔模型

目的 建立同步检测胆囊及Oddi括约肌肌电活动及胆囊、胆总管压力的动物模型.方法 对6只家兔用7F静脉深穿管分别经肝穿刺进入胆囊腔及经十二指肠腔插入胆总管.将铂金电极缝在胆囊底部浆膜上.以多通道生理仪记录家兔的胆囊及Oddi括约肌肌电信号和胆囊、胆总管压力.结果 Oddi氏括约肌肌电的峰电位＞0.05 mV,最大电位为0.26 mV,频率为0～2次/分;而慢波电位≤0.05 mV,频率为8⒍11次/分.胆囊内压力最大为15 cm H2O(6.83～15.00 cm H2O),胆总管最大压力为22 cm H2O(11～22 cm H2O).胆囊肌电活动的波形缺乏规律性.结论 兔可以作为同步检测胆囊及Oddi氏括约肌肌电活动和胆囊、胆总管压力的模型.     

胆囊切除术对家兔Oddi括约肌运动功能的影响

目的探讨胆囊切除术对家兔Oddi括约肌运动功能变化的影响。方法将16只成年家兔随机分成正常对照组、胆囊切除术组,每组8只。手术4周后进行Oddi括约肌压力及肌电的同时测定。结果压力测定:胆囊切除术组胆总管压力降低,Oddi括约肌基础压、收缩波幅升高(P<0.01);肌电测定:肌电活动由原来的锋电位变为肌电簇,波幅升高,持续时间延长(P<0.01),收缩频率未见明显变化。结论胆囊切除术后家兔Oddi括约肌功能有明显改变;Oddi括约肌蠕动增强以加快胆汁的排泄。     

犬Oddi括约肌肌电的研究

目的探索能准确稳定记录犬Oddi括约肌(sphincter of Oddi,SO)肌电活动的新方法,并对记录到的肌电波形进行初步分析。方法用自行研制的黏膜接触式电极记录30只犬SO肌电活动,同时记录十二指肠和胃的肌电活动,分析SO肌电波形的规律以及和胃十二指肠肌电的关系。结果用我们的方法可以记录到犬SO的快波和慢波,同步记录以及切离实验证实记录到的波形是犬的SO肌电而不是来自十二指肠和胃。结论犬的SO肌电记录是可行的,犬SO快波和慢波的发现将对SO功能研究提供一个新的平台。     

豚鼠急性胆囊炎对Oddi括约肌的影响

目的：观察豚鼠急性胆囊炎时Oddi括约肌形态和功能变化，探讨胆源性急性胰腺炎的发病机制。方法：英国短毛种豚鼠20只，随机分为两组，对照组（A组），开腹后浆膜接触电极测Oddi括约肌肌电活动，用4/25 powerLab压力转换系统测量胆管内压力；急性胆囊炎组（B组）开腹后胆囊内注射大肠杆菌和胆石混悬液诱发急性胆囊炎。饲养10 d后再次开腹测肌电活动和胆管及Oddi括约肌压力，并观察其病理组织学变化。结果：B组Oddi括约肌的肌电振幅、肌电簇持续时间、基础压、峰压和收缩频率明显高于A组（P＜0.01）；与A组比，B组光镜下Oddi括约肌内炎性细胞浸润，平滑肌组织排列紊乱，有较多的胶原纤维和结缔组织。结论：急性胆囊炎时，豚鼠Oddi括约肌肌电振幅、肌电簇持续时间、基础压、峰压和收缩频率明显异常，病理组织学出现炎性细胞浸润和平滑肌组织排列紊乱。     

腹腔镜胆囊切除术与内镜括约肌切开取石术联合治疗胆囊胆总管结石

目的 探讨腹腔镜胆囊切除术(LC)与内镜Oddi括约肌切开取石术(EST)联合治疗胆囊胆总管结石的临床效果.方法 回顾分析LC与EST联合治疗胆囊胆总管结石20例的临床资料、结果手术成功率95．0％，结石取净率100．0％，无并发症，平均住院7．5d结论LC与EST联合治疗胆囊胆总管结石是一种安全有效的治疗方法。     

胆囊收缩素对自体胰腺移植犬Oddi括约肌功能的影响

目的研究胆囊收缩素对胰腺移植后移植物Oddi括约肌功能的影响。方法对正常犬和膀胱引流式胰腺移植后犬应用胆囊收缩素前后进行Oddi括约肌测压。结果与正常犬相比 ,应用胆囊收缩素后Oddi括约肌的基础压、收缩频率、收缩幅度和动力指数显著降低 ,分别为 (1 8 5±2 8)mmHg与 (1 0 2± 2 2 )mmHg(P <0 0 1 )、(9 7± 1 5 )次 /min与 (5 0± 1 2 )次 /min (P <0 0 1 )、(4 7± 6 )mmHg与 (1 9± 5 )mmHg(P <0 0 1 )、(2 36± 5 6 )与 (5 0± 1 7) (P <0 0 1 )。移植物Od di括约肌基础压和收缩频率分别升高为 (2 7 8± 2 8)mmHg和 (1 3 1± 1 9)次 /min ,收缩幅度降低为(8± 2 )mmHg。移植犬应用胆囊收缩素后 ,基础压、收缩频率和动力指数分别升高为 (35 5± 5 1 )mmHg ,(1 8 9± 1 9)次 /min和 (5 1 5± 4 2 ) ,与用药前相比 ,P均 <0 0 1。 结论胆囊收缩素可抑制正常犬的Oddi括约肌运动 ,但对移植胰腺的Oddi括约肌起激动作用     

犬双侧迷走神经干切断术对Oddi括约肌肌电的影响

目的 研究双侧迷走神经干切断术对Oddi括约肌（SO）肌电的影响。方法 禁食16～18h（可自由饮水），成年杂种犬麻醉后，实验组行膈肌水平双侧迷走神经干切断术加幽门成形术，对照组仅行幽门成形术。手术后8周行SO肌电记录（SOE）。结果 实验组慢波幅度明显升高，快波未观察到显著性变化。结论 双侧迷走神经干切断术对SO肌电产生明显影响。     

一氧化氮与胆囊收缩素对犬Oddi括约肌的作用

目的 探讨一氧化氮和胆囊收缩素(CCK)在犬Oddi括约肌运动调节中的作用.方法 测定正常状态及注射CCK、硝普钠、一氧化氮合酶(NOS)抑制剂N-硝基-L-精氨酸甲酯(L-NAME)时,犬Oddi括约肌的基础压、时相收缩频率、时相收缩幅度;免疫组织化学染色法检测犬Oddi括约肌上NOS阳性神经元的表达情况.计量资料的比较采用t检验.结果 注射0、20 ng/kg CCK后,犬Oddi括约肌基础压、时相收缩频率、时相收缩幅度分别为(27±10)mm Hg(1 mm Hg=0.133 kPa)、(10±3)次/min、(32±8)mm Hg和(61±14)mm Hg、(64±21)次/min、(44±15)mm Hg;注射100 ng/kg CCK后产生最大抑制作用和最大兴奋作用时,犬Oddi括约肌基础压、时相收缩频率、时相收缩幅度分别为(77 +31)mm Hg、(69±18)次/min、(79±14)mm Hg和(140±21)mm Hg、(129±25)次/min、( 173±63)mm Hg.胆总管滴注硝普钠后,犬Oddi括约肌基础压、时相收缩幅度均下降(t =3.706,5.183,P＜0.05).而注射L-NAME后,犬Oddi括约肌基础压、时相收缩幅度均升高(t=5.859,3.588,P＜0.05).结论 20 ng/kg生理剂量的CCK可舒张犬Oddi括约肌,大剂量CCK可兴奋犬Oddi括约肌;一氧化氮对犬Oddi括约肌发挥舒张效应,此效应可能在CCK的抑制通路中发挥重要作用.     

胆囊切除对大白兔奥狄氏括约肌运动影响的实验研究

关于胆囊切除对奥狄氏括约肌生理影响的研究甚少 ,本实验对大白兔施行胆囊切除 ,并对胆囊切除前后奥狄氏括约肌的肌电活动进行短时间的检测分析 ,以间接了解实验条件下胆囊切除是否会引起奥狄氏括约肌功能紊乱 ,现报告如下。1　材料和方法实验动物大白兔 2 0只 (由山东大学齐鲁医院动物实验中心提供 ) ,雌雄不限 ,体重 2 .5～ 3ｋｇ ,禁食 12小时后 ,用乌拉坦静脉麻醉 ,气管插管 ,建立静脉通道 ,滴注生理盐水。腹部正中切口入腹 ,显露胆囊与十二指肠连接部的奥狄氏括约肌 ,将特制的双极电极插入奥狄氏括约肌浆膜下 ,固定后 ,用浸有石蜡油的…     

腹腔镜联合内窥镜治疗胆囊胆总管结石

目的 :评价腹腔镜联合内窥镜治疗胆囊胆总管结石的临床疗效。方法 :6 0例胆囊胆总管结石患者经逆行胰胆管造影 (ERCP) ,切开Oddi括约肌 (EST) ,网篮取石和气囊排石后 ,再行腹腔镜胆囊切除术(LC)。结果 :手术成功率为 80 % ,结石取净率为 10 0 % ,无严重并发症。术后住院 3～ 12d。结论 :腹腔镜联合内窥镜治疗胆囊胆总管结石的临床疗效可靠     

The cholecysto-sphincter of Oddi reflex

Multiple factors including hormonal and neural influences as well as intravascular volume, body temperature, and pharmacologic agents have been shown to influence sphincter of Oddi function. Recent studies have also suggested that mechanical or electrical stimulation of the gallbladder and the degree of gallbladder filling may affect the frequency and amplitude of sphincter of Oddi phasic contractions. However, the effect of gallbladder filling on sphincter of Oddi phasic wave direction has not previously been studied. In acute terminal experiments, eight adult male prairie dogs underwent cannulation of the gallbladder 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-tipped catheter. The distal port of this catheter was positioned in the sphincter of Oddi (SO) while the proximal port was in the distal common bile duct (CBD). Distal CBD and SO phasic wave activity was recorded first with the gallbladder perfused with lactated Ringer's solution at 0.1 ml/min (mean intragallbladder pressure 8.1 ± 0.3 mm Hg) and then with the gallbladder (GB) empty. Sphincter of Oddi phasic wave frequency was 6.7 ± 0.9/min with the GB full and 5.4 ± 0.6/min with the GB empty (P < 0.02). Phasic wave amplitude was also greater with the GB full versus empty in both the distal CBD (6.4 ± 0.6 vs 4.3 ± 0.5 mm Hg, P < 0.05) and the SO (9.5 ± 1.5 vs 6.4 ± 0.8, P = 0.075). Baseline pressures and the direction of phasic waves were unaffected by the degree of gallbladder filling. It is concluded that the degree of gallbladder filling reflexly influences sphincter of Oddi phasic wave activity and should be considered in future studies of the choledochoduodenal junction.     

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.     

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.     

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.     

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.     

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.     

A new method for correlating pancreatic and biliary duct pressures and sphincter of Oddi electromyography

Myoelectric activity of the sphincter of Oddi and duodenum was correlated with pancreatic and biliary duct pressures in eight opossums, in both the fasted and fed states. Four bipolar electrode pairs were implanted in the sphincter of Oddi and duodenum. A polyethylene T tube was placed in the pancreatic duct. The common duct was cannulated through a small bile duct. This method allowed pressure recording for several weeks and avoided interference with the flow of bile or pancreatic juice into the duodenum. The frequency of slow waves was the same in the sphincter of Oddi and duodenum (19 per minute). The variation in the frequency of spike potentials in the sphincter of Oddi correlated to that of the migrating myoelectric complex in the duodenum. The average frequency of slow waves that have superimposed spike potentials in the sphincter of Oddi and duodenum was 3.0 and 0 in phase 1, 4.7, and 6.2 in phase II, 6.1 and 15.1 in phase III, and 3.4 and 6.3 in phase IV, respectively. The average duration of a migrating myoelectric complex cycle was 92 minutes. After feeding, the interdigestive phases of the migrating myoelectric complex were abolished and substituted by a feeding activity pattern that was characterized by an average number of sphincter of Oddi and duodenum spikes of 6.6 and 10.7, respectively. The mean fasting pressure in the pancreatic and biliary duct was 15 and 13 mmHg, respectively. Pressure changes were of two types--synchronous with respiratory movements and with each sphincter of Oddi spike potential. There was no variation in the baseline pressure during the migrating myoelectric complex phases and the fed state. It is concluded that the sphincter of Oddi of the fasting opossum exhibits cyclic changes in the number of spike potentials that correlate with the migrating myoelectric complex in the duodenum. However, the number and amplitude of spike potentials are different in the sphincter of Oddi and duodenum. There is no change in the baseline pressure during fasting and feeding states, and a temporary pressure elevation synchronic with each sphincter of Oddi spike potential was observed.     

Stasis before gallstone formation: Altered gallbladder compliance or cystic duct resistance?

Gallbladder stasis occurs before gallstone formation and provides the link between the hepatic secretion of supersaturated bile and cholesterol cholelithiasis. We recently observed that cystic duct resistance increases while sphincter of Oddi resistance is unchanged in the presence of lithogenic bile without gallstones. Whether alterations in gallbladder function also lead to gallbladder stasis has been unclear. Therefore, we tested the hypothesis that before gallstone formation, stasis results from increased cystic duct resistance and altered gallbladder compliance. Adult, male prairie dogs were fed either a trace cholesterol (control) or a 0.4 percent cholesterol-enriched diet. Cystic duct resistance increased but gallbladder compliance was unchanged before gallstone formation. A significant correlation (p < 0.001) was found between the lithogenic index and cystic duct resistance in pregallstone animals. We conclude that increased resistance to flow across the cystic duct, and not altered gallbladder compliance, is etiologically related to bile stasis, an important event in gallstone formation.     

放射性核素动态扫描计量分析对胆囊切除术后胆汁排泄的评价

目的　探讨胆囊切除术对胆汁排泄的影响,寻找评价奥狄（ Ｏｄｄｉ） 括约肌功能的无创方法。 方法　将４５ 名自愿者病人随机分成３ 组,即术前组、术后组及排泄延迟组。经禁食８ ～１２ 小时后,分别静脉给予９ ９ ｍ Ｔｃ Ｅ Ｈ Ｉ Ｄ Ａ１８５ Ｍ Ｂｑ ,同时进行动态采集。取肝总管、胆总管、胆囊及十二指肠等部位的兴趣区（ｒｅｇｉｏｎ ｏｆｉｎｔｅｒｅｓｔ, Ｒ Ｏ Ｉ） ,通过实时的核素比值,分析单位时间的核素分布,同时比较胆总管兴趣区核素排泄的 Ｔｍａｘ 值。 结果　术前组与术后组比较,十二指肠与胆总管兴趣区的核素比值（ Ｒ２） 及胆总管 Ｒ Ｏ Ｉ的 Ｔｍａｘ 值差异无显著意义（ Ｐ＞ ００５） 。而排泄延迟组虽经 Ｂ 型超声检查证实无胆总管扩张,但其 Ｒ２ 值和胆总管 Ｒ Ｏ Ｉ的 Ｔｍａｘ 值与术前组对比差异有显著意义（ｔ１ ＝ ２１６ ,ｔ２ ＝ ２２９ ,ｔ３ ＝ ２０７ , Ｐ＜ ００５） 。 结论　在没有肝外梗阻,无 Ｏｄｄｉ 括约肌功能失调的病人,其胆汁排泄于术前、术后无明显变化,胆囊切除术后胆总管无代偿性扩张。肝胆放射性核素动态扫描计量分析可作为 Ｏｄｄｉ 括约肌功能失调的诊断和分型的敏感、无创方法。     

Sphincter of Oddi response to caerulein after endoscopic sphincterotomy for papillary stenosis

Using a percutaneous transhepatic cholangioscopy (PTCS) catheter, sphincter of Oddi motility was measured in a patient with papillary stenosis secondary to bile duct stones. Prior to sphincterotomy, intramuscular injection of 20 micrograms caerulein did not inhibit pathological contraction waves of the sphincter of Oddi or relieve abdominal pain. Endoscopic sphincterotomy of the lower segment of the sphincter of Oddi resulted in recovery of the normal response to caerulein, i.e. relaxation of the sphincter of Oddi. This observation indicates that the pathological contraction and lack of relaxation to cholecystokinin in a patient with papillary stenosis is due to high common bile duct pressure. The measurement of motility of sphincter of Oddi via the PTCS route is useful in diagnosing motor disorders in the sphincter of Oddi and is helpful in deciding to perform endoscopic sphincterotomy.