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Motility of the biliary system

Wylie J. Dodds, Walter J. Hogan, Joseph E. Geenen

10.1002/cphy.cp060128

Source: Supplement 16: Handbook of Physiology, The Gastrointestinal System, Motility and Circulation

Originally published: 1989

Published online: January 2011

Full Article on Wiley Online Library



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 127a)
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 127a)
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 18
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 18
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. 166
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. 59. 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. 59. 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. 170. 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. 170. 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. 169
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 85
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. 192
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. 145
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. 205. 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. 204
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. 72
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. 72
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. 204
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. 192
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. 205. 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 127a)


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 127a)


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 18


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 18


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. 166


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. 59. 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. 59. 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. 170. 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. 170. 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. 169


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 85


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. 192


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. 145


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. 205. 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. 204


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. 72


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. 72


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. 204


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. 192


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. 205. 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.

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Article Title: Motility of the biliary system
 

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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