Comprehensive Physiology Wiley Online Library

Motility of the biliary system

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Abstract

The sections in this article are:

1 Historical Background
2 Anatomy of Biliary‐Pancreatic Duct System
2.1 Gross Structure
2.2 Microscopic Structure
2.3 Species Variation
3 Methods of Study
3.1 Imaging Studies
3.2 Flow Measurements
3.3 Manometry
3.4 Electromyography
3.5 Scintigraphy
3.6 Sonography
3.7 Miscellaneous
4 Pharmacology
5 Physiology
5.1 Hepatic Bile
5.2 Gallbladder
5.3 Cystic Duct
5.4 Common Duct
5.5 Sphincter of Oddi
5.6 Overview
6 Abnormal Function In Humans
6.1 Gallbladder
6.2 Sphincter of Oddi
7 Summary
Figure 1. Figure 1.

Gross anatomy of gallbladder and bile ducts.

Adapted from Netter a)
Figure 2. Figure 2.

Embryology of pancreaticobiliary tree. A: ventral (V) and dorsal (D) pancreas arise as anlage from duodenum. B: biliary and pancreatic anlagen rotate counterclockwise (arrow) so ventral pancreas lies posterior to dorsal pancreas. C: ventral and dorsal pancreas along with their ducts fuse so duct of Wirsung (W) becomes major pancreatic duct and distal part of duct of Santorini (S) becomes accessory pancreatic duct. GB, gallbladder; CBD common bile duct.

Adapted from Netter a)
Figure 3. Figure 3.

Schematic anatomical representation of human sphincter of Oddi. Sphincter of Oddi is characterized by muscularis propria distinct from that of duodenum. Boyden observed localized areas of muscle thickening that he termed sphincter ampullae, sphincter choledochus, and sphincter pancreaticus. Common channel or ampulla is generally present.

Adapted from Boyden
Figure 4. Figure 4.

Species variation in sphincter of Oddi anatomy. CBD, common bile duct; PD, pancreatic duct; T. musc., tunica muscularis; Sph. chol., sphincter choledochus; Sph. amp., sphincter ampullae; Sph. pap., sphincter pancreaticus T. subm., tunica submucosa; T. muc., tunica mucosa.

Adapted from Boyden
Figure 5. Figure 5.

A, B, C, D: sequential radiographic images of common duct and sphincter of Oddi segment. Images taken ∼8–10 s apart. Subject was without biliary tract symptoms. Surgical clips from previous cholecystectomy. In A and C, sphincter segment is relaxed and filled, whereas sphincter is contracted and empty in B and D.

Figure 6. Figure 6.

Hysteresis loops of volume‐pressure relationships for baboon gallbladder. A: before and after administration of cholecys‐tokinin (CCK). B: before and after administration of atropine.

Adapted from Schoetz et al.
Figure 7. Figure 7.

Manometric recording of station pull‐through across sphincter of Oddi (SO) segment. Upper tracing from catheter orifice withdrawn across sphincter; lower tracing recorded from duodenal catheter taped to endoscope. Each dot represents a 2‐ to 3‐mm withdrawal of cannulating catheter. Margins of sphincter segment shown by arrows. Small pressure fluctuations caused by respiration. For tracing analysis, pressure may be measured from common bile duct (CBD) as well as from duodenum and CBD‐duodenal gradient calculated. Within sphincter, basal (base‐line) pressure is only few mmHg greater than common duct pressure. Superimposed on basal SO pressure are phasic pressure waves ∼100 mmHg in amplitude.

From Geenen et al. . Reprinted with permission of The American Gastroenterological Association, copyright 1980
Figure 8. Figure 8.

Recording of electromyographic activity from opossum sphincter of Oddi (SO). One electrode positioned on common bile duct (CBD), four along (SO) segment, and one on duodenum. Tracing shows 3 spontaneous spike‐burst sequences originating in proximal sphincter (SO4) and traversing entire SO segment. Two spike bursts, seen in duodenum, occur independently of SO myoelectrical activity.

Figure 9. Figure 9.

Measurement of gallbladder volume by sonographic method in single subject. Axial and transverse gallbladder images obtained at 10‐min intervals before and after fatty meal. Estimates for gallbladder volume calculated by sums‐of‐cylinder and ellipsoid methods were comparable. Here gallbladder emptied ∼85% of its volume within 30 min after fatty meal (Lipomul, 1.5 ml/kg). During this interval, net emptying rate was ∼1 ml/min.

Figure 10. Figure 10.

Effect of cholecystokinin octapeptide (CCK‐8) on sphincter of Oddi contractile activity. Pressure recordings obtained at endoscopic retrograde cholangiopancreatography manometry are for sphincter and duodenum. Intravenous administration of CCK‐8 associated with prompt inhibition of phasic contractions followed 30 s later by contractile activity in duodenum. CCK‐8 also depressed basal sphincter pressure by few mmHg, but this change cannot be appreciated from figure due to high pressure scale used for sphincter tracing.

From Geenen et al. . Reprinted with permission of The American Gastroenterological Association, copyright 1980
Figure 11. Figure 11.

Hepatic production of bile acids during duodenal migratory motor complex (MMC) cycle in dogs. Data plotted as mean ± 1 SD for 10 MMC cycles. Pooled data indicate that hepatic secretion of bile was generally maximal late in duodenal MMC cycle.

From Scott et al. . Reprinted with permission of The American Gastroenterological Association, copyright 1984
Figure 12. Figure 12.

Example of variations in hepatic secretion of bile acids in fasted dog. Bile acid secretion given in micromoles per minute. Electrodes distributed along entire length of small bowel. Cyclic changes observed in hepatic secretion of bile acid. Volume of bile paralleled bile acid secretion. In this example, peak bile production occurred during phase II of duodenal MMC.

From Scott et al. . Reprinted with permission of The American Gastroenterological Association, copyright 1984
Figure 13. Figure 13.

Graph of common duct bile flow in cholecystectomized dogs. Pooled data obtained from 14 migratory motor complex (MMC) cycles while extrahepatic circulation of bile acids was intact. Bile flow and bile acid secretion plotted against percent migration time of phase III activity through small bowel. Bold line indicates position of phase III activity in small bowel. Thus at 50% of migration time, phase III activity has migrated 80% of bowel length. Hepatic bile flow and bile acid secretion become maximal as phase III activity reaches midileum.

From Scott et al.
Figure 14. Figure 14.

Periodic contractions of canine gallbladder during fasting. Implanted transducers record motor contractions from gastric antrum, duodenum, and gallbladder. Three complete cycles of migratory motor complex (MMC) seen in antrum and duodenum. Gallbladder contracts during each MMC cycle, just before phase III activity front passes through duodenum.

From Itoh and Takahashi
Figure 15. Figure 15.

Relationship between gallbladder (GB) volume and gastrointestinal migrating myoelectrical complex (MMC). Histograms plotted for spike‐burst activity in gastric antrum (GA), duodenum (sites D1 and D2), sphincter of Oddi (SO), proximal jejunum (J1), and distal jejunum (J2). Four phase III MMC activity fronts occurred during 7‐h recording. Periodic changes in gallbladder volume occurred synchronously with MMC cycles.

From Takahashi et al.
Figure 16. Figure 16.

Bile duct diameter in a model of distal common duct obstruction in dogs. Sonographic measurements obtained of common duct (CD) and hepatic duct (HD). Dots represent mean values; solid lines are extrapolated curves. A: duct diameter after acute obstruction. CD and HD diameter demonstrated substantial increase within 2 days followed by slower increase that continued for several weeks or longer. B: duct diameter after release of common duct obstruction that was maintained for more than 1 wk. Decrease in common duct diameter slower than rate of dilation and some residual distension remains, 6 mm vs. normal value of 2 mm. If obstruction was released in less than 1 wk, however, common duct returned to normal preobstruction diameter.

From Raptopoulos et al.
Figure 17. Figure 17.

Multilumen manometric recording from human sphincter of Oddi (SO). Three recording sites spaced at 2‐mm intervals located in sphincter, with fourth recording site in duodenum. Three spontaneous peristaltic contraction waves occur that migrate antegrade toward duodenum and traverse entire sphincter segment. Normally ∼60% of phasic sphincter contractions migrate antegrade, whereas remainder either migrate retrograde or occur simultaneously at all sites.

From Toouli et al. . Reprinted with permission of The American Gastroenterological Association, copyright 1982
Figure 18. Figure 18.

Station pull‐through across opossum sphincter of Oddi (SO). Sample tracings shown for sites indicated by dots. High‐pressure zone (HPZ) seen only in distal SO segment. This HPZ did not exhibit transient relaxations to common duct pressure. Phasic pressure waves occurred along entire sphincter segment but not in common bile duct (CBD). Phasic pressure waves of maximal amplitude occurred in distal half of sphincter. Wave amplitude decreases progressively toward proximal sphincter margin. Contraction waves not recorded in common duct.

From Toouli et al.
Figure 19. Figure 19.

Concurrent recording of electrical and manometric activity from opossum sphincter of Oddi (SO) and duodenum. Manometric catheter with three orifices spaced at 5‐mm intervals was positioned in sphincter so that each recording orifice was at same level as bipolar electrode. Site SO3 located in proximal sphincter. Electrical spike burst occurs at each site immediately before upstroke onset of peristaltic manometric pressure wave. In sequence shown, one of contractions at SO3 does not traverse entire sphincter.

Figure 20. Figure 20.

Myoelectric and contractile activity recorded concurrently from intact sphincter of Oddi (SO) segment in vitro. At regular intervals, phasic contractions originate in proximal SO and propagate antegrade toward duodenum, indicated by dashed line. Each phasic contraction was associated with electrical control complex. When control‐wave propagation was incomplete, as occurred in alternate sequences, propagation of phasic contraction was incomplete. CBD, common bile duct; PD, papillary duct.

From Helm et al.
Figure 21. Figure 21.

Contractile activity recorded from muscle rings sectioned from sphincter of Oddi (SO). Rings contract spontaneously at random with respect to one another. Proximal‐to‐distal gradient of inherent contraction frequencies is evident. CBD, common bile duct; PD, papillary duct.

From Helm et al.
Figure 22. Figure 22.

Relation between sphincter of Oddi (SO) peristaltic sequence recorded by cineradiography, electromyography, and intraluminal manometry. At given sphincter level, spike burst occurs just prior to upstroke onset of peristaltic pressure wave. Onset of contraction pinches off bolus, thereby giving its tail an inverted‐V configuration. Passage of tail by a given site corresponds to upstroke of pressure wave. Pressure within bolus, ahead of major manometric pressure complex, ramps up slightly until pressure is reached that overcomes resistance of narrow nozzle. Contrast medium is then pushed into duodenum. Each peristaltic sequence in sphincter interrupts passive bile duct emptying for an interval of ∼6 s. CD, common duct.

Figure 23. Figure 23.

Bile duct emptying drawn from images of cineradiographic recording. Catheter positioned in proximal common bile duct (CBD) for infusing contrast not shown. Time in seconds given above images of contrast material. In this example, contrast medium flowed into CBD at rate of ∼6 drops/min (0.1 ml/min) from reservoir. Before sphincter of Oddi (SO) peristalsis, contrast flowed into CBD, which then emptied passively into SO segment. Drops (gtts) indicate CBD outflow as well as CBD inflow. During 2‐s interval, SO peristalsis actively expelled contrast from SO segment into duodenum. Zone of narrowing observed in distal SO segment. During passage of SO contraction wave, SO segment was pinched off from CBD, thereby interrupting passive CBD outflow into SO segment. After SO emptying, short 4‐s interval of delayed SO filling persisted until SO contraction was complete. When pressure in SO segment returned to initial value after peristalsis, fluid flow from CBD into SO recommenced, leading to passive SO filling during SO diastole. Cycle repeated itself with onset of next SO peristaltic contraction.

From Toouli et al.
Figure 24. Figure 24.

Myoelectrical spike‐burst activity in sphincter of Oddi and gastrointestinal tract of fasted awake opossum. Electrodes positioned on duodenum (sites D1 and D2), sphincter of Oddi (SO), and jejunum (J). Phase III activity of migrating myoelectrical complex (MMC) passes from duodenum to jejunum. Spike‐burst activity of sphincter of Oddi is continuous but intensifies and reaches maximal rate concurrent with passage of phase III MMC activity front through duodenum.

Figure 25. Figure 25.

Effect of feeding on sphincter of Oddi contractile activity and gallbladder volume. Concurrent electrical recordings (spike bursts (SB)/min) obtained from gastric antrum (GA), duodenum (sites D1 and D2), sphincter of Oddi (SO), proximal jejunum (J1), and distal jejunum (J2). Animal was fed after two spontaneous cycles of migratory myoelectric complex during fasting. Feeding abolished fasting pattern of myoelectric activity and elicited continuous feed pattern of spike‐burst activity in sphincter of Oddi, stomach, and small bowel. Substantial gallbladder emptying occurred within 40 min after eating, and gallbladder remained contracted for at least several hours.

From Takahashi et al.
Figure 26. Figure 26.

Manometric recording from patient with sphincter of Oddi (SO) stenosis. Three sphincter recording sites show phasic sphincter contraction superimposed on hypertensive basal sphincter pressure of ∼30–45 mmHg above intraduodenal pressure. Short bars indicate reference for zero atmosphere pressure. Amyl nitrite inhalation abolished phasic sphincter contractions but had no effect on increased basal sphincter pressure. Failure of smooth muscle relaxant to substantially decrease elevated basal pressure indicates that increased pressure is caused by organic abnormality, such as fibrosis, rather than functional sphincter spasm.

Figure 27. Figure 27.

Manometric recording from human sphincter of Oddi (SO). A: normal response of sphincter of Oddi to cholecystokinin octapeptide (CCK‐8), which abolishes phasic contractions and reduces basal SO pressure. B: paradoxical response of sphincter of Oddi to CCK‐8 in patient with suspected obstructive sphincter dysfunction. Prior to CCK‐8 administration, basal sphincter pressure is elevated. CCK caused paradoxical sphincter contraction consisting of increase in basal pressure and rate of phasic contractions. Concurrent with paradoxical sphincter contraction to CCK‐8, patient complained of upper abdominal pain.

Figure 28. Figure 28.

Manometric recording from human sphincter of Oddi (SO). Phasic sphincter contractions were primarily retrograde in this patient with retained, nonobstructing calculus in common duct. R, retrograde contraction; S, simultaneous contraction.

From Toouli et al. . Reprinted with permission of The American Gastroenterological Association, copyright 1982
Figure 29. Figure 29.

Manometric recording from the human sphincter of Oddi (SO). Tachyoddia was observed in this patient with suspected obstructive sphincter dysfunction. Rate of phasic sphincter contractions was 10–12/min, compared with normal range of 2–8/min.



Figure 1.

Gross anatomy of gallbladder and bile ducts.

Adapted from Netter a)


Figure 2.

Embryology of pancreaticobiliary tree. A: ventral (V) and dorsal (D) pancreas arise as anlage from duodenum. B: biliary and pancreatic anlagen rotate counterclockwise (arrow) so ventral pancreas lies posterior to dorsal pancreas. C: ventral and dorsal pancreas along with their ducts fuse so duct of Wirsung (W) becomes major pancreatic duct and distal part of duct of Santorini (S) becomes accessory pancreatic duct. GB, gallbladder; CBD common bile duct.

Adapted from Netter a)


Figure 3.

Schematic anatomical representation of human sphincter of Oddi. Sphincter of Oddi is characterized by muscularis propria distinct from that of duodenum. Boyden observed localized areas of muscle thickening that he termed sphincter ampullae, sphincter choledochus, and sphincter pancreaticus. Common channel or ampulla is generally present.

Adapted from Boyden


Figure 4.

Species variation in sphincter of Oddi anatomy. CBD, common bile duct; PD, pancreatic duct; T. musc., tunica muscularis; Sph. chol., sphincter choledochus; Sph. amp., sphincter ampullae; Sph. pap., sphincter pancreaticus T. subm., tunica submucosa; T. muc., tunica mucosa.

Adapted from Boyden


Figure 5.

A, B, C, D: sequential radiographic images of common duct and sphincter of Oddi segment. Images taken ∼8–10 s apart. Subject was without biliary tract symptoms. Surgical clips from previous cholecystectomy. In A and C, sphincter segment is relaxed and filled, whereas sphincter is contracted and empty in B and D.



Figure 6.

Hysteresis loops of volume‐pressure relationships for baboon gallbladder. A: before and after administration of cholecys‐tokinin (CCK). B: before and after administration of atropine.

Adapted from Schoetz et al.


Figure 7.

Manometric recording of station pull‐through across sphincter of Oddi (SO) segment. Upper tracing from catheter orifice withdrawn across sphincter; lower tracing recorded from duodenal catheter taped to endoscope. Each dot represents a 2‐ to 3‐mm withdrawal of cannulating catheter. Margins of sphincter segment shown by arrows. Small pressure fluctuations caused by respiration. For tracing analysis, pressure may be measured from common bile duct (CBD) as well as from duodenum and CBD‐duodenal gradient calculated. Within sphincter, basal (base‐line) pressure is only few mmHg greater than common duct pressure. Superimposed on basal SO pressure are phasic pressure waves ∼100 mmHg in amplitude.

From Geenen et al. . Reprinted with permission of The American Gastroenterological Association, copyright 1980


Figure 8.

Recording of electromyographic activity from opossum sphincter of Oddi (SO). One electrode positioned on common bile duct (CBD), four along (SO) segment, and one on duodenum. Tracing shows 3 spontaneous spike‐burst sequences originating in proximal sphincter (SO4) and traversing entire SO segment. Two spike bursts, seen in duodenum, occur independently of SO myoelectrical activity.



Figure 9.

Measurement of gallbladder volume by sonographic method in single subject. Axial and transverse gallbladder images obtained at 10‐min intervals before and after fatty meal. Estimates for gallbladder volume calculated by sums‐of‐cylinder and ellipsoid methods were comparable. Here gallbladder emptied ∼85% of its volume within 30 min after fatty meal (Lipomul, 1.5 ml/kg). During this interval, net emptying rate was ∼1 ml/min.



Figure 10.

Effect of cholecystokinin octapeptide (CCK‐8) on sphincter of Oddi contractile activity. Pressure recordings obtained at endoscopic retrograde cholangiopancreatography manometry are for sphincter and duodenum. Intravenous administration of CCK‐8 associated with prompt inhibition of phasic contractions followed 30 s later by contractile activity in duodenum. CCK‐8 also depressed basal sphincter pressure by few mmHg, but this change cannot be appreciated from figure due to high pressure scale used for sphincter tracing.

From Geenen et al. . Reprinted with permission of The American Gastroenterological Association, copyright 1980


Figure 11.

Hepatic production of bile acids during duodenal migratory motor complex (MMC) cycle in dogs. Data plotted as mean ± 1 SD for 10 MMC cycles. Pooled data indicate that hepatic secretion of bile was generally maximal late in duodenal MMC cycle.

From Scott et al. . Reprinted with permission of The American Gastroenterological Association, copyright 1984


Figure 12.

Example of variations in hepatic secretion of bile acids in fasted dog. Bile acid secretion given in micromoles per minute. Electrodes distributed along entire length of small bowel. Cyclic changes observed in hepatic secretion of bile acid. Volume of bile paralleled bile acid secretion. In this example, peak bile production occurred during phase II of duodenal MMC.

From Scott et al. . Reprinted with permission of The American Gastroenterological Association, copyright 1984


Figure 13.

Graph of common duct bile flow in cholecystectomized dogs. Pooled data obtained from 14 migratory motor complex (MMC) cycles while extrahepatic circulation of bile acids was intact. Bile flow and bile acid secretion plotted against percent migration time of phase III activity through small bowel. Bold line indicates position of phase III activity in small bowel. Thus at 50% of migration time, phase III activity has migrated 80% of bowel length. Hepatic bile flow and bile acid secretion become maximal as phase III activity reaches midileum.

From Scott et al.


Figure 14.

Periodic contractions of canine gallbladder during fasting. Implanted transducers record motor contractions from gastric antrum, duodenum, and gallbladder. Three complete cycles of migratory motor complex (MMC) seen in antrum and duodenum. Gallbladder contracts during each MMC cycle, just before phase III activity front passes through duodenum.

From Itoh and Takahashi


Figure 15.

Relationship between gallbladder (GB) volume and gastrointestinal migrating myoelectrical complex (MMC). Histograms plotted for spike‐burst activity in gastric antrum (GA), duodenum (sites D1 and D2), sphincter of Oddi (SO), proximal jejunum (J1), and distal jejunum (J2). Four phase III MMC activity fronts occurred during 7‐h recording. Periodic changes in gallbladder volume occurred synchronously with MMC cycles.

From Takahashi et al.


Figure 16.

Bile duct diameter in a model of distal common duct obstruction in dogs. Sonographic measurements obtained of common duct (CD) and hepatic duct (HD). Dots represent mean values; solid lines are extrapolated curves. A: duct diameter after acute obstruction. CD and HD diameter demonstrated substantial increase within 2 days followed by slower increase that continued for several weeks or longer. B: duct diameter after release of common duct obstruction that was maintained for more than 1 wk. Decrease in common duct diameter slower than rate of dilation and some residual distension remains, 6 mm vs. normal value of 2 mm. If obstruction was released in less than 1 wk, however, common duct returned to normal preobstruction diameter.

From Raptopoulos et al.


Figure 17.

Multilumen manometric recording from human sphincter of Oddi (SO). Three recording sites spaced at 2‐mm intervals located in sphincter, with fourth recording site in duodenum. Three spontaneous peristaltic contraction waves occur that migrate antegrade toward duodenum and traverse entire sphincter segment. Normally ∼60% of phasic sphincter contractions migrate antegrade, whereas remainder either migrate retrograde or occur simultaneously at all sites.

From Toouli et al. . Reprinted with permission of The American Gastroenterological Association, copyright 1982


Figure 18.

Station pull‐through across opossum sphincter of Oddi (SO). Sample tracings shown for sites indicated by dots. High‐pressure zone (HPZ) seen only in distal SO segment. This HPZ did not exhibit transient relaxations to common duct pressure. Phasic pressure waves occurred along entire sphincter segment but not in common bile duct (CBD). Phasic pressure waves of maximal amplitude occurred in distal half of sphincter. Wave amplitude decreases progressively toward proximal sphincter margin. Contraction waves not recorded in common duct.

From Toouli et al.


Figure 19.

Concurrent recording of electrical and manometric activity from opossum sphincter of Oddi (SO) and duodenum. Manometric catheter with three orifices spaced at 5‐mm intervals was positioned in sphincter so that each recording orifice was at same level as bipolar electrode. Site SO3 located in proximal sphincter. Electrical spike burst occurs at each site immediately before upstroke onset of peristaltic manometric pressure wave. In sequence shown, one of contractions at SO3 does not traverse entire sphincter.



Figure 20.

Myoelectric and contractile activity recorded concurrently from intact sphincter of Oddi (SO) segment in vitro. At regular intervals, phasic contractions originate in proximal SO and propagate antegrade toward duodenum, indicated by dashed line. Each phasic contraction was associated with electrical control complex. When control‐wave propagation was incomplete, as occurred in alternate sequences, propagation of phasic contraction was incomplete. CBD, common bile duct; PD, papillary duct.

From Helm et al.


Figure 21.

Contractile activity recorded from muscle rings sectioned from sphincter of Oddi (SO). Rings contract spontaneously at random with respect to one another. Proximal‐to‐distal gradient of inherent contraction frequencies is evident. CBD, common bile duct; PD, papillary duct.

From Helm et al.


Figure 22.

Relation between sphincter of Oddi (SO) peristaltic sequence recorded by cineradiography, electromyography, and intraluminal manometry. At given sphincter level, spike burst occurs just prior to upstroke onset of peristaltic pressure wave. Onset of contraction pinches off bolus, thereby giving its tail an inverted‐V configuration. Passage of tail by a given site corresponds to upstroke of pressure wave. Pressure within bolus, ahead of major manometric pressure complex, ramps up slightly until pressure is reached that overcomes resistance of narrow nozzle. Contrast medium is then pushed into duodenum. Each peristaltic sequence in sphincter interrupts passive bile duct emptying for an interval of ∼6 s. CD, common duct.



Figure 23.

Bile duct emptying drawn from images of cineradiographic recording. Catheter positioned in proximal common bile duct (CBD) for infusing contrast not shown. Time in seconds given above images of contrast material. In this example, contrast medium flowed into CBD at rate of ∼6 drops/min (0.1 ml/min) from reservoir. Before sphincter of Oddi (SO) peristalsis, contrast flowed into CBD, which then emptied passively into SO segment. Drops (gtts) indicate CBD outflow as well as CBD inflow. During 2‐s interval, SO peristalsis actively expelled contrast from SO segment into duodenum. Zone of narrowing observed in distal SO segment. During passage of SO contraction wave, SO segment was pinched off from CBD, thereby interrupting passive CBD outflow into SO segment. After SO emptying, short 4‐s interval of delayed SO filling persisted until SO contraction was complete. When pressure in SO segment returned to initial value after peristalsis, fluid flow from CBD into SO recommenced, leading to passive SO filling during SO diastole. Cycle repeated itself with onset of next SO peristaltic contraction.

From Toouli et al.


Figure 24.

Myoelectrical spike‐burst activity in sphincter of Oddi and gastrointestinal tract of fasted awake opossum. Electrodes positioned on duodenum (sites D1 and D2), sphincter of Oddi (SO), and jejunum (J). Phase III activity of migrating myoelectrical complex (MMC) passes from duodenum to jejunum. Spike‐burst activity of sphincter of Oddi is continuous but intensifies and reaches maximal rate concurrent with passage of phase III MMC activity front through duodenum.



Figure 25.

Effect of feeding on sphincter of Oddi contractile activity and gallbladder volume. Concurrent electrical recordings (spike bursts (SB)/min) obtained from gastric antrum (GA), duodenum (sites D1 and D2), sphincter of Oddi (SO), proximal jejunum (J1), and distal jejunum (J2). Animal was fed after two spontaneous cycles of migratory myoelectric complex during fasting. Feeding abolished fasting pattern of myoelectric activity and elicited continuous feed pattern of spike‐burst activity in sphincter of Oddi, stomach, and small bowel. Substantial gallbladder emptying occurred within 40 min after eating, and gallbladder remained contracted for at least several hours.

From Takahashi et al.


Figure 26.

Manometric recording from patient with sphincter of Oddi (SO) stenosis. Three sphincter recording sites show phasic sphincter contraction superimposed on hypertensive basal sphincter pressure of ∼30–45 mmHg above intraduodenal pressure. Short bars indicate reference for zero atmosphere pressure. Amyl nitrite inhalation abolished phasic sphincter contractions but had no effect on increased basal sphincter pressure. Failure of smooth muscle relaxant to substantially decrease elevated basal pressure indicates that increased pressure is caused by organic abnormality, such as fibrosis, rather than functional sphincter spasm.



Figure 27.

Manometric recording from human sphincter of Oddi (SO). A: normal response of sphincter of Oddi to cholecystokinin octapeptide (CCK‐8), which abolishes phasic contractions and reduces basal SO pressure. B: paradoxical response of sphincter of Oddi to CCK‐8 in patient with suspected obstructive sphincter dysfunction. Prior to CCK‐8 administration, basal sphincter pressure is elevated. CCK caused paradoxical sphincter contraction consisting of increase in basal pressure and rate of phasic contractions. Concurrent with paradoxical sphincter contraction to CCK‐8, patient complained of upper abdominal pain.



Figure 28.

Manometric recording from human sphincter of Oddi (SO). Phasic sphincter contractions were primarily retrograde in this patient with retained, nonobstructing calculus in common duct. R, retrograde contraction; S, simultaneous contraction.

From Toouli et al. . Reprinted with permission of The American Gastroenterological Association, copyright 1982


Figure 29.

Manometric recording from the human sphincter of Oddi (SO). Tachyoddia was observed in this patient with suspected obstructive sphincter dysfunction. Rate of phasic sphincter contractions was 10–12/min, compared with normal range of 2–8/min.

References
 1. Acosta, J. M., F. Civantos, G. L. Nardi, and B. Castelman. Fibrosis of the papilla of Vater. Surg. Gynecol. Obstet. 124: 787–794, 1967.
 2. Babbitt, D. P., R. J. Starshak, and A. R. Clemett. Choledochal cyst: a concept of etiology. Am. J. Roentgenol. Rad. Ther. Nucl. Med. 119: 57–62, 1973.
 3. Bar‐Meir, S., J. E. Geenen, W. J. Hogan, W. J. Dodds, E. T. Stewart, and R. C. Arndorfer. Biliary and pancreatic duct pressures measured by ERCP manometry in patients with suspected papillary stenosis. Dig. Dis. Sci. 24: 209–213, 1979.
 4. Bar‐Meir, S., and Z. Halpern. The significance of the diameter of the common bile duct in cholecystectomized patients. Am. J. Gastroenterol. 79: 59–60, 1984.
 5. Bar‐Meir, S., Z. Halpern, and E. Bardan. Nitrate therapy in a patient with papillary dysfunction. Am. J. Gastroenterol. 78: 94–95, 1983.
 6. Bar‐Meir, S., Z. Halpern, E. Bardan, and T. Gilat. Frequency of papillary dysfunction among cholecystectomized patients. Hepatology Baltimore 4: 328–330, 1984.
 7. Becker, J. M., W. M. Duff, and F. G. Moody. Myoelectric control of gastrointestinal and biliary motility: a review. Surgery St. Louis 89: 466–477, 1981.
 8. Becker, J. M., F. G. Moody, and A. R. Zinsmeister. Effect of gastrointestinal hormones on the biliary sphincter of the opossum. Gastroenterology 82: 1300–1307, 1982.
 9. Behar, J., and P. Biancani. Neural control of the feline gallbladder. In: Gastrointestinal Motility, edited by J. Christensen. New York: Raven, 1980, p. 97–109.
 10. Behar, J., and P. Biancani. Effect of cholecystokinin and the octapeptide of cholecystokinin on the feline sphincter of Oddi and gallbladder. Mechanisms of action. J. Clin. Invest. 66: 1231–1239, 1980.
 11. Behar, J., and P. Biancani. Effect of motilin on the cat sphincter of Oddi (SO): mechanism of action (Abstract). Gastroenterology 84: 1102, 1983.
 12. Behar, J., and P. Biancani. Neural control of the sphincter of Oddi. Gastroenterology 86: 134–141, 1984.
 13. Beneventano, T. C., H. G. Jacobson, E. S. Hurwitt, and C. J. Schein. Cine‐cholangiomanometry: physiologic observations. Am. J. Roentgenol. Radium Ther. Nucl. Med. 100: 673–679, 1967.
 14. Berk, R. N. Cholecystokinin cholecystography in the diagnosis of chronic acalculous cholecystitis and biliary dyskinesia. A critical appraisal. Gastrointest. Radiol. 1: 325–330, 1977.
 15. Björck, S., H. Ahlman, and A. Dahlström. Effect of extrinsic denervation on the rate of net water transport of the feline gall bladder. Gut 25: 603–610, 1984.
 16. Björck, S., R. Jansson, and J. Svanvik. Adrenergic influence on concentrating function in the feline gall bladder. Gut 23: 1019–1023, 1982.
 17. Bobba, V. R., G. T. Krishnamurthy, E. Kingston, F. E. Turner, P. H. Brown, and K. Langrell. Gallbladder dynamics induced by a fatty meal in normal subjects and patients with gallstones. J. Nucl. Med. 25: 21–24, 1984.
 18. Boyden, E. A. The sphincter of Oddi in man and certain representative mammals. Surgery St. Louis 1: 25–37, 1937.
 19. Boyden, E. A. The anatomy of the choledochoduodenal junction in man. Surg. Gynecol. Obstet. 104: 641–652, 1957.
 20. Braverman, D. Z., M. L. Johnson, and F. Kern, Jr. Effects of pregnancy and contraceptive steroids on gallbladder function. N. Engl. J. Med. 302: 362–364, 1980.
 21. Bueno, L., and F. Praddaude. Electrical activity of the gallbladder and biliary tract in sheep and its relationship with antral and duodenal motility. Ann. Biol. Anim. Biochim. Biophys. 19: 1109–1121, 1979.
 22. Burnett, W., F. W. Gairns, and P. Bacsich. Some observations on the innervation of the extrahepatic biliary system in man. Ann. Surg. 159: 8–26, 1964.
 23. Cai, W. Q., and G. Gabella. The musculature of the gallbladder and biliary pathways in the guinea pig. J. Anat. 136: 237–250, 1983.
 24. Caroli, J., P. Porcher, G. Pequignot, and M. Delattre. Contribution of cineradiography to study of the function of the human biliary tract. Am. J. Dig. Dis. 5: 677–696, 1960.
 25. Carr‐Locke, D. L., and J. A. Gregg. Endoscopic manometry of pancreatic and biliary sphincter zones in man. Basal results in healthy volunteers. Dig. Dis. Sci. 26: 7–15, 1981.
 26. Cattell, R. B., B. P. Colcock, and J. L. Pollack. Stenosis of the sphincter of Oddi. N. Engl. J. Med. 256: 429–435, 1957.
 27. Chang, T. M., and W. Y. Chey. Radioimmunoassay of cholecystokinin. Dig. Dis. Sci. 28: 456–468, 1983.
 28. Chang, V. H., J. J. Cunningham, and J. J. Fromkes. Sonographic measurement of the extrahepatic bile duct before and after retrograde cholangiography. Am. J. Roentgenol. Radium. Ther. Nucl. Med. 144: 753–755, 1985.
 29. Clave, R. A., and M. R. Gasper. Incidence of gallbladder disease after vagotomy. Am. J. Surg. 118: 169–176, 1969.
 30. Coelho, J. C., F. G. Moody, and N. Senniger. A new method for correlating pancreatic and biliary duct pressures and sphincter of Oddi electromyography. Surgery St. Louis 97: 342–349, 1985.
 31. Cohn, M. S., S. I. Schwartz, W. W. Faloon, and J. T. Adams. Effect of sphincteroplasty on gallbladder function and bile composition. Ann. Surg. 189: 317–321, 1979.
 32. Courtney, D. F., A. S. Clanachan, and G. W. Scott. Cholecystokinin constricts the canine cystic duct. Gastroenterology 85: 1154–1159, 1983.
 33. Cox, K. L., A. T. W. Cheung, E. M. Walsh, and C. K. Iwahashi‐Hosoda. Choledochoduodenal junction (CDJ) dysmotility associated with cholelithiasis and hydrops of the gallbladder (Abstract). Dig. Dis. Sci. 30: 765, 1985.
 34. Cox, K. L., A. T. W. Cheung, E. M. Walsh, C. K. Iwahashi‐Hosoda, and C. L. Lohse. Intravital microscopy: a new in vivo method for quantitating biliary motility (Abstract). Dig. Dis. Sci. 30: 766, 1985.
 35. Csendes, A., A. Kruse, P. Funch‐Jensen, M. J. Oster, J. Ornsholt, and E. Amdrup. Pressure measurements in the biliary and pancreatic duct systems in controls and in patients with gallstones, previous cholecystectomy, or common bile duct stones. Gastroenterology 77: 1203–1210, 1979.
 36. Csendes, A., and A. Sepulveda. Intraluminal gallbladder pressure measurements in patients with chronic or acute cholecystitis. Am. J. Surg. 139: 383–384, 1980.
 37. Davison, J. S., and M. Al‐Hassani. The role of noncholinergic, nonadrenergic nerves in regulating the distensibility of the guinea pig gallbladder. In: Gastrointestinal Motility, edited by J. Christensen. New York: Raven, 1980, p. 89–95.
 38. Davison, J. S., and S. Fosel. Interactions between vagus nerve stimulation and pentagastrin or secretin on the guinea pig gallbladder. Digestion 13: 251–254, 1975.
 39. Debas, H. T., and T. Yamagishi. Evidence for a pylorocholecystic reflex for gallbladder contraction. Ann. Surg. 190: 170–175, 1979.
 40. Dodds, W. J., W. J. Groh, R. M. A. Darweesh, T. L. Lawson, S. M. A. Kishk, and M. K. Kern. Sonographic measurement of gallbladder volume. Am. J. Roentgenol. Radium Ther. Nucl. Med. 145: 1009–1011, 1985.
 41. Doty, J. E., H. A. Pitt, S. L. Kuchenbecker, and L. Den Besten. Impaired gallbladder emptying before gallstone formation in the prairie dog. Gastroenterology 85: 168–174, 1983.
 42. Du Bois, F. S., and E. A. Hunt. Peristalsis of the common bile duct in the opossum. Anat. Rec. 53: 387–397, 1932.
 43. Edholm, P. Gallbladder evacuation in the normal male induced by cholecystokinin. Acta Radiol. 53: 257–265, 1960.
 44. Escourrou, J., J. A. Cordova, F. Lazorthes, J. Frexinos, and A. Ribet. Early and late complications after endoscopic sphincterotomy for biliary lithiasis with and without the gall bladder ‘in situ’. Gut 25: 598–602, 1984.
 45. Everson, G. T., D. Z. Braverman, M. L. Johnson, and F. Kern, Jr. A critical evaluation of real‐time ultrasonography for the study of gallbladder volume and contraction. Gastroenterology 79: 40–46, 1980.
 46. Everson, G. T., C. McKinley, M. Lawson, M. Johnson, and F. Kern, Jr. Gallbladder function in the human female: effect of the ovulatory cycle, pregnancy, and contraceptive steroids. Gastroenterology 82: 711–719, 1982.
 47. Ferrari, B. T., R. L. O'Halloran, W. P. Longmire, Jr., and K. J. Lewin. Atypical papillary hyperplasia of the pancreatic duct mimicking obstructing pancreatic carcinoma. N. Engl. J. Med. 301: 531–532, 1979.
 48. Ferrucci, J. T., Jr., J. Wittenberg, L. B. Stone, and J. R. Dreyfuss. Hypotonic cholangiography with glucagon. Radiology 118: 466–467, 1976.
 49. Fisher, R. S., E. Rock, and L. S. Malmud. Cholinergic effects on gallbladder emptying in humans. Gastroenterology 89: 716–722, 1985.
 50. Fisher, R. S., F. Stelzer, E. Rock, and L. S. Malmud. Abnormal gallbladder emptying in patients with gallstones. Dig. Dis. Sci. 27: 1019–1024, 1982.
 51. Foesel, S., and K. F. Sewing. Enhancement of electrically stimulated guinea pig gallbladder contraction by subthreshold concentrations of gastrointestinal hormones in vitro. Experientia Basel 34: 205–206, 1978.
 52. Fridhandler, T. M., J. S. Davison, and E. A. Shaffer. Defective gallbladder contractility in the ground squirrel and prairie dog during the early stages of cholesterol gallstone formation. Gastroenterology 85: 830–836, 1983.
 53. Fried, G. M., W. D. Ogden, C. J. Fagan, I. Wiener, K. Inoue, G. H. Greeley, Jr., and J. C. Thompson. Comparison of cholecystokinin release and gallbladder emptying in men and in women at estrogen and progesterone phases of the menstrual cycle. Surgery St. Louis 95: 284–289, 1984.
 54. Fried, G. M., W. D. Ogden, J. Swierczek, G. H. Greeley, Jr., P. L. Rayford, and J. C. Thompson. Release of cholecystokinin in conscious dogs: correlation with simultaneous measurements of gallbladder pressure and pancreatic protein secretion. Gastroenterology 85: 1113–1119, 1983.
 55. Funch‐Jensen, P., P. Diederich, and K. Kraglund. Intraoperative sphincter of Oddi manometry in patients with gallstones. Scand. J. Gastroenterol. 19: 931–936, 1984.
 56. Funch‐Jensen, P., K. Kraglund, and J. C. Djurhuus. The influence of measuring catheter diameter on direct manometry in the canine sphincter of Oddi. Scand. J. Gastroenterol. 19: 926–930, 1984.
 57. Funch‐Jensen, P., K. Kraglund, and J. C. Djurhuus. Multimodal contractile activity of the canine sphincter of Oddi. Eur. Surg. Res. 16: 312–316, 1984.
 58. Funch‐Jensen, P., H. Stødkilde‐Jørgensen, K. Kraglund, and N. A. Lovgreen. Biliary manometry in dogs. Digestion 22: 89–93, 1981.
 59. Geenen, J. E., W. J. Hogan, W. J. Dodds, E. T. Stewart, and R. C. Arndorfer. Intraluminal pressure recording from the human sphincter of Oddi. Gastroenterology 78: 317–324, 1980.
 60. Geenen, J. E., W. J. Hogan, R. D. Shaffer, E. T. Stewart, W. J. Dodds, and R. C. Arndorfer. Endoscopic electrosurgical papillotomy and manometry in biliary tract disease. J. Am. Med. Assoc. 237: 2075–2078, 1977.
 61. Geenen, J. E., W. J. Hogan, E. T. Stewart, W. J. Dodds, and R. C. Arndorfer. ERCP manometry of the sphincter of Oddi. In: The Papilla Vateri and Its Diseases, edited by M. Classen et al. Koln, FRG: Witzstrock, 1979, p. 92–98.
 62. Geenen, J., W. Hogan, J. Toouli, W. Dodds, and R. Venu. A prospective randomized study of the efficacy of endoscopic sphincterotomy for patients with presumptive sphincter of Oddi dysfunction (Abstract). Gastroenterology 86: 1086, 1984.
 63. Gilsdorf, R. B. The effect of simulated gallstones on gallbladder pressures and bile flow response to eating. Surg. Gynecol. Obstet. 138: 161–168, 1974.
 64. Goldberg, H. I. Cholecystokinin cholecystography. Semin. Roentgenol. 11: 175–179, 1976.
 65. Gregg, J. A., and D. L. Carr‐Locke. Endoscopic pancreatic and biliary manometry in pancreatic, biliary, and papillary disease, and after endoscopic sphincterotomy and surgical sphincteroplasty. Gut 25: 1247–1254, 1984.
 66. Guelrud, M., S. Mendoza, S. Vicent, M. Gomez, and B. Villalta. Pressures in the sphincter of Oddi in patients with gallstones, common duct stones, and recurrent pancreatitis. J. Clin. Gastroenterol. 5: 37–41, 1983.
 67. Guelrud, M., and J. H. Siegel. Hypertensive pancreatic duct sphincter as a cause of pancreatitis. Dig. Dis. Sci. 29: 225–231, 1984.
 68. Gullo, L., L. Bolondi, P. Priori, P. Casanova, and G. Labo. Inhibitory effect of atropine on cholecystokinin‐induced gallbladder contraction in man. Digestion 29: 209–213, 1984.
 69. Hallenbeck, G. A. Biliary and pancreatic intraductal pressures. In: Handbook of Physiology. Alimentary Canal. Secretion, edited by C. F. Code. Washington, DC: Am. Physiol. Soc., 1967, sect. 6, vol. II, chapt. 57, p. 1007–1025.
 70. Hand, B. H. An anatomical study of the choledochoduodenal area. Br. J. Surg. 50: 486–494, 1963.
 71. Helm, J. F., J. Christensen, W. J. Dodds, and S. Sarna. Intrinsic innervation of the opossum sphincter of Oddi (SO) (Abstract). Gastroenterology 84: 1185, 1983.
 72. Helm, J. F., W. J. Dodds, J. Christensen, and S. K. Sarna. Control mechanism of spontaneous in vitro contractions of the opossum sphincter of Oddi. Am. J. Physiol. 249 (Gastrointest. Liver Physiol. 12): G572–G579, 1985.
 73. Hess, W. Manometry and radiography in the biliary system during surgery. In: Endoscopic Sphincterotomy of the Papilla Vateri, edited by L. Demling and M. Classen. Littleton, MA: PSG, 1978.
 74. Hess, W. Physiology of the sphincter of Oddi. In: Endoscopic Sphincterotomy of the Papilla Vateri, edited by L. Demling and M. Classen. Littleton, MA: PSG, 1978.
 75. Hogan, W. J., W. J. Dodds, and J. E. Geenen. Motor function of the biliary‐duct system. In: A Guide to Gastrointestinal Motility, edited by J. Christensen, D. L. Wingate, and R. A. Gregory. Bristol, UK: Wright, 1983, p. 157–197.
 76. Hogan, W. J., J. Geenen, W. J. Dodds, J. Toouli, R. Venu, and J. Helm. Paradoxical motor response to cholecystokinin (CCK‐OP) in patients with suspected sphincter of Oddi dysfunction (Abstract). Gastroenterology 82: 1085, 1982.
 77. Hogan, W. J., J. E. Geenen, J. Kruidenier, R. Venu, J. Helm, W. J. Dodds, and S. D. Wilson. Ineffectiveness of conventional sphincteroplasty in relieving pancreatic duct sphincter pressure in patients with idiopathic recurrent pancreatitis (Abstract). Gastroenterology 84: 1189, 1983.
 78. Hogan, W. J., J. Geenen, R. Venu, W. J. Dodds, J. Helm, and J. Toouli. Abnormally rapid phasic contractions of the human sphincter of Oddi (tachyoddia) (Abstract). Gastroenterology 84: 1189, 1983.
 79. Honda, R., J. Toouli, W. J. Dodds, S. Sarna, W. J. Hogan, and Z. Itoh. Relationship of sphincter of Oddi spike bursts to gastrointestinal myoelectric activity in conscious opossums. J. Clin. Invest. 69: 770–778, 1982.
 80. Hopton, D., and T. T. White. Effect of hepatic and celiac vagal stimulation on common bile‐duct pressure. Am. J. Dig. Dis. 16: 1095–1101, 1971.
 81. Hutton, S. W., C. E. Sievert, Jr., J. A. Vennes, and W. C. Duane. The effect of sphincterotomy on gallstone formation in the prairie dog. Gastroenterology 81: 663–667, 1981.
 82. Ihasz, M., and C. A. Griffith. Gallstones after vagotomy. Am. J. Surg. 141: 48–50, 1981.
 83. Inberg, M. V., and M. Vuorio. Human gallbladder function after selective gastric and total abdominal vagotomy. Acta Chir. Scand. 135: 625–633, 1969.
 84. Ishioka, T. Electromyographic study of the choledochoduodenal junction and duodenal wall muscle. Tohoku J. Exp. Med. 70: 73–84, 1959.
 85. Itoh, Z., and I. Takahashi. Periodic contractions of the canine gallbladder during the interdigestive state. Am. J. Physiol. 240 (Gastrointest. Liver Physiol. 3): G183–G189, 1981.
 86. Ivy, A. C., and E. Oldberg. A hormone mechanism for gallbladder contraction and evacuation. Am. J. Physiol. 86: 599–613, 1928.
 87. Jansson, R., E. Thornell, and J. Svanvik. Effects of indomethacin on gallbladder pressure in patients with acute cholecystitis. Scand. J. Urol. Nephrol. 75: 51–53, 1983.
 88. Jones, R. S., and M. I. Grossman. Choleretic effects of cholecystokinin, gastrin II, and caerulein in the dog. Am. J. Physiol. 219: 1014–1018, 1970.
 89. Kelly, T. R., and P. E. Swaney. Gallstone pancreatitis: the second time around. Surgery St. Louis 92: 571–575, 1982.
 90. Kern, F., Jr., G. T. Everson, B. De Mark, C. McKinley, R. Showalter, W. Erfling, D. Z. Braverman, P. Szczepanik‐van Leeuwen, and P. D. Klein. Biliary lipids, bile acids and gallbladder function in the human female. Effects of pregnancy and the ovulatory cycle. J. Clin. Invest. 68: 1229–1242, 1981.
 91. Kern, M. K., J. H. Linehan, W. J. Dodds, I. Takahashi, and W. J. Hogan. Mathematical modeling of pressure‐flow kinetics of the opossum sphincter of Oddi (Abstract). Gastroenterology 86: 1133, 1984.
 92. Kraglund, K., J. Hjermind, F. T. Jensen, H. Stødkilde‐Jørgensen, E. Oster‐Jørgensen, and S. A. Pedersen. Gallbladder emptying and gastrointestinal cyclic motor activity in humans. Scand. J. Gastroenterol. 19: 990–994, 1984.
 93. Krishnamurthy, G. T., V. R. Bobba, and E. Kingston. Radionuclide ejection fraction: a technique for quantitative analysis of motor function of the human gallbladder. Gastroenterology 80: 482–490, 1981.
 94. Kyosola, K. Cholinesterase histochemistry of the innervation of the smooth muscle sphincters around the terminal intramural part of the ductus choledochus in the cat and the dog. Acta Physiol. Scand. 90: 278–280, 1974.
 95. Kyosola, K. Biliary dyskinesia. Ann. Chir. Gynaecol. Fenn. 64: 189–194, 1975.
 96. Kyosola, K. Adrenergic and cholinergic innervation of the supraduodenal common bile duct. Am. J. Gastroenterol. 70: 179–183, 1978.
 97. Kyosola, K. Sympatho‐adrenergic neural control of the sphincter of Oddi of the cat and the dog. Tohoku J. Exp. Med. 127: 113–117, 1979.
 98. Kyosola, K., and L. Rechardt. The anatomy and innervation of the sphincter of Oddi in the dog and cat. Am. J. Anat. 140: 497–521, 1974.
 99. La Morte, W. W., D. J. Schoetz, Jr., D. H. Birkett, and L. F. Williams, Jr. The role of the gallbladder in the pathogenesis of cholesterol gallstones. Gastroenterology 77: 580–592, 1979.
 100. Lawson, M., G. T. Everson, W. Klingensmith, and F. Kern, Jr. Coordination of gastric and gallbladder emptying after ingestion of a regular meal. Gastroenterology 85: 866–870, 1983.
 101. Lee, R. G., J. A. Gregg, A. M. Koroshetz, T. C. Hill, and M. E. Clouse. Sphincter of Oddi stenosis: diagnosis using hepatobiliary scintigraphy and endoscopic manometry. Radiology 156: 793–796, 1985.
 102. Leese, T., J. P. Neoptolemos, and D. L. Carr‐Locke. Successes, failures, early complications and their management following endoscopic sphincterotomy: results in 394 consecutive patients from a single centre. Br. J. Surg. 72: 215–219, 1985.
 103. Lichtenstein, M. E., and A. C. Ivy. The function of the “valves” of Heister. Surgery St. Louis 1: 38–52, 1937.
 104. Liedberg, G., and M. Halabi. The effect of vagotomy on flow resistance at the choledocho‐duodenal junction. Acta Chir. Scand. 136: 208–212, 1970.
 105. Lilja, P., C. J. Fagan, I. Wiener, K. Inoue, L. C. Watson, P. L. Rayford, and J. C. Thompson. Infusion of pure cholecystokinin in humans. Gastroenterology 83: 256–261, 1982.
 106. Low‐Beer, T. S., R. F. Harvey, E. R. Davies, and A. F. Read. Abnormalities of serum cholecystokinin and gallbladder emptying in celiac disease. N. Engl. J. Med. 292: 961–963, 1975.
 107. Ludwick, J. R., and P. Bass. Contractile and electric activity of the extrahepatic biliary tract and duodenum. Surg. Gynecol. Obstet. 124: 536–546, 1967.
 108. MacPherson, B. R., G. W. Scott, J. P. Chansouria, and A. W. Fisher. The muscle layer of the canine gallbladder and cystic duct. Acta Anat. 120: 117–122, 1984.
 109. Mann, F. C. A comparative study of the anatomy of the sphincter at the duodenal end of the common bile‐duct with special reference to species of animals without a gall‐bladder. Anat. Rec. 18: 355–360, 1920.
 110. Mann, F. C. A study of the tonicity of the sphincter at the duodenal end of the common bile duct. J. Lab. Clin. Med. 5: 107–110, 1920.
 111. Maton, P. N., A. C. Selden, M. L. Fitzpatrick, and V. S. Chadwick. Infusion of cholecystokinin octapeptide in man: relation between plasma cholecystokinin concentrations and gallbladder emptying rates. Eur. J. Clin. Invest. 14: 37–41, 1984.
 112. Maton, P. N., A. C. Selden, M. L. Fitzpatrick, and V. S. Chadwick. Defective gallbladder emptying and cholecystokinin release in celiac disease. Gastroenterology 88: 391–396, 1985.
 113. Matsumoto, T., S. K. Sarna, and R. E. Condon. Gallbladder electrical activity in vivo (Abstract). Gastroenterology 88: 1493, 1985.
 114. Matsumoto, T., S. K. Sarna, R. E. Condon, and W. J. Dodds. Gallbladder cyclic motor activity (Abstract). Gastroenterology 88: 1493, 1985.
 115. Maudgal, D. P., R. M. Kupfer, P. L. Zentler‐Munro, and T. C. Northfield. Postprandial gallbladder emptying in patients with gall stones. Br. Med. J. 280: 141–143, 1980.
 116. McMaster, P. D., and R. Elman. On the expulsion of bile by the gallbladder and a reciprocal relationship with the sphincter activity. J. Exp. Med. 44: 173–198, 1926.
 117. Meltzer, S. J. The disturbance of the law of contrary innervation as a pathogenetic factor in the diseases of the bile ducts and the gall bladder. Am. J. Med. Sci. 153: 469–477, 1917.
 118. Meshkinpour, H., M. Mollot, G. B. Eckerling, and L. Bookman. Bile duct dyskinesia. A clinical and manometric study. Gastroenterology 87: 759–762, 1984.
 119. Mok, H. Y., K. von Bergmann, and S. M. Grundy. Kinetics of the enterohepatic circulation during fasting: biliary lipid secretion and gallbladder storage. Gastroenterology 78: 1023–1033, 1980.
 120. Moody, F. G., J. M. Becker, and J. R. Potts. Transduodenal sphincteroplasty and transampullary septectomy for postcholecystectomy pain. Ann. Surg. 197: 627–636, 1983.
 121. Mueller, P. R., J. T. Ferrucci, Jr., J. F. Simeone, E. van Sonnenberg, D. A. Hall, and J. Wittenberg. Observations on the distensibility of the common bile duct. Radiology 142: 467–472, 1982.
 122. Muller, E. L., M. A. Lewinski, and H. A. Pitt. The cholecysto‐sphincter of Oddi reflex. J. Surg. Res. 36: 377–383, 1984.
 123. Nakayama, S., and H. Fukuda. Conduction of activity between muscles in the terminal region of the common bile duct and in the neighboring duodenum. Acta Med. Okayama 30: 21–35, 1976.
 124. Nardi, G. L. Papillitis and stenosis of the sphincter of Oddi. Surg. Clin. N. Am. 53: 1149–1160, 1973.
 125. Nathan, M. H., A. Newman, J. McFarland, and D. J. Murray. Cholecystokinin cholecystography. Radiology 93: 1–8, 1969.
 126. Nebel, O. T. Manometric evaluation of the papilla of Vater. Gastrointest. Endosc. 21: 126–128, 1975.
 127. Neschis, M., M. C. King, and R. A. Murphy. Cholecystokinin cholecystography in the diagnosis of acalculous extra‐hepatic biliary tract disorders. Am. J. Gastroenterol. 70: 593–599, 1978.
 128. Netter, F. H. The CIBA Collection of Medical Illustrations. Summit, NJ: Ciba Pharm., 1953, vol. 5, pt. 3.
 129. Northfield, T. C., R. M. Kupfer, D. P. Maudgal, P. L. Zentler‐Munro, S. T. Meller, N. W. Garvie, and R. McCready. Gall‐bladder sensitivity to cholecystokinin in patients with gall stones. Br. Med. J. 280: 143–144, 1980.
 130. Novis, B. H., P. C. Bornman, A. W. Girdwood, and I. N. Marks. Endoscopic manometry of the pancreatic duct and sphincter zone in patients with chronic pancreatitis. Dig. Dis. Sci. 30: 225–228, 1985.
 131. O'Brien, J. J., E. A. Shaffer, L. F. Williams, Jr., D. M. Small, J. Lynn, and J. Wittenberg. A physiological model to study gallbladder function in primates. Gastroenterology 67: 119–125, 1974.
 132. Oddi, R. D'une disposition a sphincter de l'ouverture du canal choledogue. Arch. Ital. Biol. 8: 317–322, 1887.
 133. [Transl. from Italian] J. Gastroenterol. 17: 109–111, 1985.
 134. Ono, K., N. Watanabe, K. Suzuki, H. Tsuchida, Y. Sugiyama, and M. Abo. Bile flow mechanism in man. Arch. Surg. 96: 869–874, 1968.
 135. Opie, E. L. The etiology of acute hemorrhagic pancreatitis. Johns Hopkins Hosp. Bull. 12: 182–188, 1901.
 136. Oster, M. J., A. Csendes, P. Funch‐Jensen, and H. Skjoldborg. Intraoperative pressure measurements of the choledochoduodenal junction, common bile duct, cysticocholedochal junction and gallbladder in humans. Surg. Gynecol. Obstet. 150: 385–389, 1980.
 137. Otto, W. J., G. W. Scott, and C. M. Rodkiewicz. A comparison of resistances to flow through the cystic duct and the sphincter of Oddi. J. Surg. Res. 27: 68–72, 1979.
 138. Parry, E. W., G. A. Hallenbeck, and J. H. Grindlay. Pressures in the pancreatic and common ducts. Arch. Surg. 70: 757–765, 1955.
 139. Peeters, T. L., G. R. Vantrappen, and J. Janssens. Bile acid output and the interdigestive migrating motor complex in normals and in cholecystectomy patients. Gastroenterology 79: 678–681, 1980.
 140. Persson, C. G. Adrenergic, cholecystokinetic and morphine‐induced effects on extra‐hepatic biliary motility. Acta Physiol. Scand. Suppl. 383: 1–32, 1972.
 141. Persson, C. G. Inhibitory innervation of cat sphincter of Oddi. Br. J. Pharmacol. 58: 479–482, 1976.
 142. Pitt, H. A., J. E. Doty, and L. Den Besten. Increased intragallbladder pressure response to cholecystectokinin‐octapeptide following vagotomy and pyloroplasty. J. Surg. Res. 35: 325–331, 1983.
 143. Pitt, H. A., J. E. Doty, L. Den Besten, and S. L. Kuchenbecker. Stasis before gallstone formation: altered gallbladder compliance or cystic duct resistance? Am. J. Surg. 143: 144–149, 1982.
 144. Pitt, H. A., J. E. Doty, J. J. Roslyn, and L. Den Besten. The role of altered extrahepatic biliary function in the pathogenesis of gallstones after vagotomy. Surgery St. Louis 90: 418–425, 1981.
 145. Pitt, H. A., J. J. Roslyn, S. L. Kuchenbecker, J. E. Doty, and L. Den Besten. The role of cystic duct resistance in the pathogenesis of cholesterol gallstones. J. Surg. Res. 30: 508–514, 1981.
 146. Pomeranz, I. S., and E. A. Shaffer. Abnormal gallbladder emptying in a subgroup of patients with gallstones. Gastroenterology 88: 787–791, 1985.
 147. Raptopoulos, V., T. M. Fabian, W. Silva, C. J. D'Orsi, A. Karellas, C. C. Compton, F. J. Krolikowski, P. Doherty, and E. H. Smith. The effect of time and cholecystectomy of experimental biliary tree dilatation. Invest. Radiol. 20: 276–286, 1985.
 148. Richter, J. M., R. H. Schapiro, A. G. Mulley, and A. L. Warshaw. Association of pancreas divisum and pancreatitis, and its treatment by sphincteroplasty of the accessory ampulla. Gastroenterology 81: 1104–1110, 1981.
 149. Rosch, W., H. Koch, and L. Demling. Manometric studies during ERCP and endoscopic papillotomy. Endoscopy 8: 30–33, 1976.
 150. Roslyn, J. J., H. A. Pitt, L. L. Mann, M. E. Ament, and L. Den Besten. Gallbladder disease in patients on long‐term parenteral nutrition. Gastroenterology 84: 148–154, 1983.
 151. Rous, P., and P. D. McMaster. The concentrating activity of the gallbladder. J. Exp. Med. 34: 47–73, 1921.
 152. Ruckebusch, Y., and G. Soldani. Gallbladder motility in sheep: effects of cholecystokinin and related peptides. J. Vet. Pharm. Ther. 8: 263–269, 1985.
 153. Rudick, J., and J. S. Hutchison. Evaluation of vagotomy and biliary function by combined oral cholecystography and intravenous cholangiography. Ann. Surg. 162: 234–240, 1965.
 154. Ryan, J. P. Motility of the gallbladder and biliary tree. In: Physiology of the Gastrointestinal Tract, edited by L. R. Johnson. New York: Raven, 1981, p. 473–494.
 155. Ryan, J. P. Effect of pregnancy on gallbladder contractility in the guinea pig. Gastroenterology 87: 674–678, 1984.
 156. Ryan, T., C. A. Pellegrini, and L. W. Way. Bile kinetics during fasting in the prairie dog (Abstract). Gastroenterology 84: 1292, 1983.
 157. Ryan, J. P., and S. Ryave. Effect of vasoactive intestinal polypeptide on gallbladder smooth muscle in vitro. Am. J. Physiol. 234 (Endocrinol. Metab. Gastrointest. Physiol. 3): E44–E46, 1978.
 158. Salducci, J., B. Naudi, G. Pin, F. Ranieri, and H. Monges. Papilla electromyography: endoluminal recording performed in many by perduodenoscopic cannulation. In: The Sphincter of Oddi, edited by J. Delmont. New York: Karger, 1976, p. 77–79. (Proc. Gastroenterol. Symp., 3rd, Nice, Italy.)
 159. Salik, J. O., C. I. Siegel, and A. I. Mendeloff. Biliary‐duodenal dynamics in man. Radiology 106: 1–11, 1973.
 160. Sarles, J. C., P. Delecourt, H. Castello, L. Gaeta, M. Nacchiero, J. P. Amoros, M. A. Devaux, and R. Awad. Action of gastrointestinal hormones on the myoelectric activity of the sphincter of Oddi in living rabbit. Regul. Pept. 2: 113–124, 1981.
 161. Sarles, J. C., P. Delecourt, M. A. Devaux, J. P. Amoros, J. C. Guicheney, and E. Wunsch. In vivo effect of 13 Leu motilin on the electric activity of the rabbit sphincter of Oddi. Horm. Metab. Res. 13: 340–342, 1981.
 162. Sarles, J. C., A. Midejean, and M. A. Devaux. Electromyography of the sphincter of Oddi. Am. J. Gastroenterol. 63: 221–231, 1975.
 163. Sarva, R. P., D. P. Shreiner, D. Van Thiel, and N. Yingvorapant. Gallbladder function: methods for measuring filling and emptying. J. Nucl. Med. 26: 140–144, 1985.
 164. Sauerbruch, T., F. Stellaard, and G. Paumgartner. Effect of endoscopic sphincterotomy on bile acid pool size and bile lipid composition in man. Digestion 27: 87–92, 1983.
 165. Schein, C. J., and T. C. Beneventano. Choledochal dynamics in man. Surg. Gynecol. Obstet. 126: 591–596, 1968.
 166. Schein, C. J., and M. L. Gliedman. The influence of vagotomy on the normal and diseased gallbladder. Digestion 3: 243–250, 1970.
 167. Scheske, G. A., P. L. Cooperberg, M. M. Cohen, and H. J. Burhenne. Dynamic changes in the caliber of the major bile ducts related to obstruction. Radiology 135: 215–216, 1980.
 168. Schoetz, D. J., Jr., W. W. La Morte, W. E. Wise, D. H. Birkett, and L. F. Williams, Jr. Mechanical properties of primate gallbladder: description by a dynamic method. Am. J. Physiol. 241 (Gastrointest. Liver Physiol. 4): G376–G381, 1981.
 169. Scott, G. W., and W. J. Otto. Resistance and sphincter‐like properties of the cystic duct. Surg. Gynecol. Obstet. 149: 177–182, 1979.
 170. Scott, G. W., R. E. Smallwood, and S. Rowlands. Flow through the bile duct after cholecystectomy. Surg. Gynecol. Obstet. 140: 912–918, 1975.
 171. Scott, R. B., S. M. Strasberg, T. Y. El‐Sharkawy, and N. E. Diamant. Regulation of the fasting enterohepatic circulation of bile acids by the migrating myoelectric complex in dogs. J. Clin. Invest. 71: 644–654, 1983.
 172. Scott, R. B., S. M. Strasberg, T. Y. El‐Sharkawy, and N. E. Diamant. Fasting canine biliary secretion and the sphincter of Oddi. Gastroenterology 87: 793–804, 1984.
 173. Shaffer, E. A., P. McOrmond, and H. Duggan. Quantitative cholescintigraphy: assessment of gallbladder filling and emptying and duodenogastric reflux. Gastroenterology 79: 899–906, 1980.
 174. Shawker, T. H., B. L. Jones, and M. E. Girton. Distal common bile duct obstruction: an experimental study in monkeys. J. Clin. Ultrasound 9: 77–82, 1981.
 175. Silva, G. S. P. A simple method for computing the volume of the human gallbladder. Radiology 52: 94–102, 1949.
 176. Simeone, J. F., R. J. Butch, P. R. Mueller, E. van Sonnenberg, J. T. Ferrucci, Jr., D. A. Hall, D. B. Kopans, S. L. Dawson, J. Wittenberg, and K. McCarthy. The bile ducts after a fatty meal: further sonographic observations. Radiology 154: 763–768, 1985.
 177. Simeone, J. F., P. R. Mueller, J. T. Ferrucci, Jr., E. van Sonnenberg, D. A. Hall, J. Wittenberg, C. C. Neff, and R. C. O'Connell. Sonography of the bile ducts after a fatty meal: an aid in detection of obstruction. Radiology 143: 211–215, 1982.
 178. Slater, G., P. I. Tartter, D. Dreiling, A. H. Aufses, Jr., J. Rudick, D. Delman, and W. Blesser. Resistance of the canine common bile duct. Bull. NY Acad. Med. 59: 711–720, 1983.
 179. Slota, T., J. E. Geenen, W. J. Hogan, E. T. Stewart, and W. J. Dodds. The fate of common bile duct (CBD) calculi following endoscopic sphincterotomy (ES): the role of incision length and stone diameter (Abstract). Gastrointest. Endosc. 25: 50, 1979.
 180. Soon‐Shiong, P., K. L. Cox, G. L. Rosenquist, C. Iwahashi‐Hosoda, and H. Carr. Evidence of a noncholecystokinin stimulant of gallbladder contraction: comparison of fasting serum concentrations in healthy subjects and in patients with gallstones. Am. J. Surg. 149: 163–166, 1985.
 181. Spellman, S. J., E. A. Shaffer, and L. Rosenthall. Gallbladder emptying in response to cholecystokinin. A cholescintigraphic study. Gastroenterology 77: 115–120, 1979.
 182. Stasiewicz, J., and K. G. Wormsley. Functional control of the biliary tract. Acta Hepato‐Gastroenterol. 21: 450–468, 1974.
 183. Strasberg, S. M., R. N. Redinger, D. M. Small, and R. H. Egdahl. The effect of elevated biliary tract pressure on biliary lipid metabolism and bile flow in nonhuman primates. J. Lab. Clin. Med. 99: 342–353, 1982.
 184. Sundler, F., J. Alumets, R. Håkanson, S. Ingemansson, J. Fahrenkrug, and O. Schaffalitzky de Muckadell. VIP innervation of the gallbladder (Eng. Abstract). Gastroenterology 72: 1375–1377, 1977.
 185. Suzuki, T., I. Takahashi, and Z. Itoh. Motilin and gallbladder: new dimensions in gastrointestinal physiology. Peptides Fayetteville 2: 229–233, 1981.
 186. Svanvik, J., B. Allen, C. Pellegrini, R. Bernhoft, and L. Way. Variations in concentrating function of the gallbladder in the conscious monkey. Gastroenterology 86: 919–925, 1984.
 187. Svanvik, J., and R. Jansson. An experimental method for studying in vivo gallbladder absorption. Gastroenterology 72: 634–638, 1977.
 188. Svenberg, T., N. D. Christofides, M. L. Fitzpatric, F. Areola‐Ortiz, S. R. Bloom, and R. B. Welbourn. Inter‐digestive biliary output in man: relationship to fluctuations in plasma motilin and effect of atropine. Gut 23: 1024–1028, 1982.
 189. Takahashi, I., W. J. Dodds, W. J. Hogan, K. Baker, and Z. Itoh. Effect of vagotomy on changes in gallbladder volume during fasting and after feeding in the conscious opossum (Abstract). Gastroenterology 86: 1273, 1984.
 190. Takahashi, I., W. J. Dodds, W. J. Hogan, R. Layman, and Z. Itoh. Effect of proglumide on biliary‐tract contractile activity in the opossum (Abstract). Gastroenterology 86: 1274, 1984.
 191. Takahashi, I., W. J. Dodds, W. J. Hogan, and Z. Itoh. Effect of migrating myoelectric activity on the hepatic secretion of bile in the opossum (Abstract). Gastroenterology 86: 1273, 1984.
 192. Takahashi, I., W. J. Dodds, Z. Itoh, W. J. Hogan, and M. K. Kern. Influence of transsphincteric fluid flow on spike burst rate of the opossum sphincter of Oddi. Gastroenterology 87: 1292–1298, 1984.
 193. Takahashi, I., R. Honda, W. J. Dodds, S. Sarna, J. Toouli, Z. Itoh, W. Y. Chey, W. J. Hogan, D. Greiff, and K. Baker. Effect of motilin on the opossum upper gastrointestinal tract and sphincter of Oddi. Am. J. Physiol. 245 (Gastrointest. Liver Physiol. 8): G476–G481, 1983.
 194. Takahashi, I., M. K. Kern, W. J. Dodds, W. J. Hogan, S. Sarna, K. H. Soergel, and Z. Itoh. Contraction pattern of opossum gallbladder during fasting and after feeding. Am. J. Physiol. 250 (Gastrointest. Liver Physiol. 13): G227–G235, 1986.
 195. Takahashi, I., M. Nakaya, T. Suzuki, and Z. Itoh. Postprandial changes in contractile activity and bile concentration in gallbladder of the dog. Am. J. Physiol. 243 (Gastrointest. Liver Physiol. 6): G365–G371, 1982.
 196. Takahashi, I., T. Suzuki, I. Aizawa, and Z. Itoh. Comparison of gallbladder contractions induced by motilin and cholecystokinin in dogs. Gastroenterology 82: 419–424, 1982.
 197. Tanaka, M., S. Ikeda, and F. Nakayama. Continuous measurement of common bile duct pressure with an indwelling microtransducer catheter introduced by duodenoscopy: new diagnostic aid for postcholecystectomy dyskinesia—a preliminary report. Gastrointest. Endosc. 29: 83–88, 1983.
 198. Tanaka, M., S. Ikeda, and F. Nakayama. Change in bile duct pressure responses after cholecystectomy: loss of gallbladder as a pressure reservoir. Gastroenterology 87: 1154–1159, 1984.
 199. Tansy, M. F., D. L. Innes, J. S. Martin, and F. M. Kendall. The role of the intramural common bile duct in the filling of the canine gallbladder. Surg. Gynecol. Obstet. 139: 585–592, 1974.
 200. Tansy, M. F., R. C. Mackowiak, and R. B. Chaffee. A vagosympathetic pathway capable of influencing common bile duct motility in the dog. Surg. Gynecol. Obstet. 133: 225–236, 1971.
 201. Tansy, M. F., L. Salkin, D. L. Innes, J. S. Martin, F. M. Kendall, and D. Litwack. The mucosal lining of the intramural common bile duct as a determinant of ductal opening pressure. Am. J. Dig. Dis. 20: 613–625, 1975.
 202. Thompson, J. C., G. M. Fried, W. D. Ogden, C. J. Fagan, K. Inoue, I. Wiener, and L. C. Watson. Correlation between release of cholecystokinin and contraction of the gallbladder in patients with gallstones. Ann. Surg. 195: 670–676, 1982.
 203. Thune, A., E. Thornell, and J. Svanvik. Flow resistance in the choledocho‐duodenal junction is regulated by distending pressure in the biliary tract (Abstract). Gastroenterology 88: 1615, 1985.
 204. Toouli, J., J. Dent, M. Bushell, A. Wycherley, and G. Stevenson. Gallbladder (GB) emptying in relation to duodenal interdigestive migrating motor contractions (MMC) (Abstract). Gastroenterology 88: 1616, 1985.
 205. Toouli, J., W. J. Dodds, R. Honda, and W. J. Hogan. Effect of histamine on motor function of opossum sphincter of Oddi. Am. J. Physiol. 241 (Gastrointest. Liver Physiol. 4): G122–G128, 1981.
 206. Toouli, J., W. J. Dodds, R. Honda, S. Sarna, W. J. Hogan, R. A. Komorowski, J. H. Linehan, and R. C. Arndorfer. Motor function of the opossum sphincter of Oddi. J. Clin. Invest. 71: 208–220, 1983.
 207. Toouli, J., J. E. Geenen, W. J. Hogan, W. J. Dodds, and R. C. Arndorfer. Sphincter of Oddi motor activity: a comparison between patients with common bile duct stones and controls. Gastroenterology 82: 111–117, 1982.
 208. Toouli, J., W. J. Hogan, J. E. Geenen, W. J. Dodds, and R. C. Arndorfer. Action of cholecystokinin‐octapeptide on sphincter of Oddi basal pressure and phasic wave activity in humans. Surgery St. Louis 92: 497–503, 1982.
 209. Toouli, J., I. C. Roberts‐Thomson, J. Dent, and J. Lee. Manometric disorders in patients with suspected sphincter of Oddi dysfunction. Gastroenterology 88: 1243–1250, 1985.
 210. Van der Linden, W., and V. Kempi. Filling of the gallbladder as studied by computer‐assisted Tc‐99m HIDA scintigraphy: concise communication. J. Nucl. Med. 25: 292–298, 1984.
 211. Vantrappen, G. The migrating myoelectric complex. In: Motility of the Digestive Tract, edited by M. Wienbeck. New York: Raven, 1982, p. 157–167.
 212. Whitaker, L. R. The mechanism of the gall bladder. Am. J. Physiol. 78: 411–436, 1926.
 213. Wiener, I., K. Inoue, C. J. Fagan, P. Lilja, L. C. Watson, and J. C. Thompson. Release of cholecystokinin in man: correlation of blood levels with gallbladder contraction. Ann. Surg. 194: 321–327, 1981.
 214. Williams, R. D., J. C. Fish, and D. D. Williams. The significance of biliary pressure. Arch. Surg. 95: 374–379, 1967.
 215. Williams, R. D., and T. T. Huang. The effect of vagotomy on biliary pressure. Surgery St. Louis 66: 353–356, 1969.
 216. Winkelstein, A. Some observations on the entrance of bile into the duodenum. Surg. Gynecol. Obstet. 40: 545–547, 1925.
 217. Winkelstein, A., and P. W. Aschner. The mechanism of the flow of bile from the liver into the intestines. Am. J. Med. Sci. 171: 104–111, 1926.
 218. Wyatt, A. P. The relationship of the sphincter of Oddi to the stomach, duodenum and gall‐bladder. J. Physiol. Lond. 193: 225–243, 1967.
 219. Yamasato, T. Physiological and pharmacological studies on the motility of the bile duct in the chicken. Jpn. J. Smooth Muscle Res. 10: 287–297, 1974.
 220. Yau, W. M., and M. L. Youther. Modulation of gallbladder motility by intrinsic cholinergic neurons. Am. J. Physiol. 247 (Gastrointest. Liver Physiol. 10): G662–G666, 1984.
 221. Zeman, R. K., K. J. Taylor, A. T. Rosenfield, A. Schwartz, and J. A. Gold. Acute experimental biliary obstruction in the dog: sonographic findings and clinical implications. Am. J. Roentgenol. Radium Ther. Nucl. Med. 136: 965–967, 1981.

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Wylie J. Dodds, Walter J. Hogan, Joseph E. Geenen. Motility of the biliary system. Compr Physiol 2011, Supplement 16: Handbook of Physiology, The Gastrointestinal System, Motility and Circulation: 1055-1101. First published in print 1989. doi: 10.1002/cphy.cp060128