Motor function of the opossum sphincter of Oddi.

We studied the opossum sphincter of Oddi (SO) because in this species the SO is approximately 3 cm in length and its extraduodenal location permits recording of motor activity with negligible interference from duodenal motor activity. The SO segment of 120 animals was evaluated by one or more of the following: (a) intraluminal manometry; (b) electromyography; (c) common bile duct (CBD) flow monitored by a drop counter; (d) cineradiography of intraductal contrast medium; and (e) histologic examination. SO pull-throughs using an infused catheter of 0.6-mm o.d. invariably showed a high pressure zone (HPZ) of 18 +/- 3 SE mm Hg in the terminal 4-5 mm of the SO segment. This HPZ had a narrow lumen, 0.5-0.7 mm in diam, and prominent circular muscle. The HPZ in the terminal SO had both active and passive components. HPZ with minimal amplitude and a paucity of underlying smooth muscle were present inconstantly at the junction of the SO segment with the CBD and pancreatic duct, respectively. The dominant feature of the SO segment was rhythmic peristaltic contractions that originated in the proximal SO and propagated toward the duodenum. These contractions occurred spontaneously at a rate of 2-8/min, ranged up to 200 mm Hg in magnitude, had a duration of approximately 5 s and were not abolished by tetrodotoxin. Concurrent myoelectric and manometric recordings showed that each phasic contraction was immediately preceded by an electrical spike burst. Simultaneous recordings of cineradiography, CBD inflow of contrast medium, SO manometry, and SO electromyography indicated that rhythmic peristaltic contractions stripped contrast medium from the SO into the duodenum. During SO systole, CBD emptying was transiently interrupted, whereas SO filling occurred during the diastolic interval between SO peristaltic contractions. SO distention increased the frequency of SO peristalsis. We conclude that (a) the dominant feature of the opossum SO is rhythmic peristaltic contractions that originate in the proximal SO and propagate toward the duodenum; (b) these forceful SO peristaltic contractions are myogenic in origin and serve as a peristaltic pump that actively empties the SO segment; (c) CBD outflow occurs passively during SO diastole, but is interrupted transiently during each SO peristaltic contraction; and (d) a short HPZ with active as well as passive components exists in the distal SO segment and acts as a variable resistor to SO outflow.

Relationship of sphincter of Oddi spike bursts to gastrointestinal myoelectric activity in conscious opossums.

The oppossum sphincter of Oddi (SO) exhibits peristaltic spike bursts with accompanying contraction waves that originate proximally in the sphincter of Oddi and propagate toward the duodenum. In this study we recorded myoelectrical activity of the opossum SO and upper gastrointestinal tract in six conscious animals using chronically implanted electrodes. Biopolar electrodes were implanted in the gastric antrum, duodenum, SO segment, jejunum, and ileum. During fasting the frequency of SO spike bursts, scored as number per minute, showed a cyclic pattern consisting of four phases (A to D). Phase A had a low spike burst frequency of approximately 2/min that lasted approximately 20 min. In phase B, the spike burst frequency increased progressively during a 40-45 min interval culminating in a short interval of phase C activity characterized by a maximal spike burst frequency of approximately 5/min. During phase D, the spike bursts decreased over 15 min to merge with the low frequency of phase A and the cycle repeated. Cycle length of the interdigestive SO cycle, 87+/-11 SD min, was virtually identical with that of the interdigestive migrating myoelectric complex (MMC) of the upper gastrointestinal tract. The onset of phase C activity in the SO began 1-2 min before phase III of the MMC activity in the duodenum. Feeding abolished the cyclic pattern of spike burst activity in the SO as well as in the upper gastrointestinal tract. After feeding the SO spike bursts occurred at a frequency of 5-6/min for at least 3 h. We conclude that: (a) During fasting, the oppossum SO exhibits cyclic changes in its spike burst frequency; (b) Maximal spike burst frequency of the SO occurs virtually concurrent with passage of phase III MMC activity through the duodenum and; (c) Feeding abolishes the interdigestive cyclic spike burst pattern of the SO as well as that of the gastrointestinal tract.

Vasoactive intestinal polypeptide mediates cholecystokinin-induced relaxation of the sphincter of Oddi.

This study evaluates the hypothesis that cholecystokinin (CCK) relaxes the sphincter of Oddi via vasoactive intestinal polypeptide (VIP). Isolated canine sphincter of Oddi were suspended in organ baths under standard conditions. Responses to cholecystokinin octapeptide (CCK-8) and VIP were recorded on a pen recorder via an isometric transducer. 10(-11)-10(-7) M CCK-8 and 4 X 10(-11)-5 X 10(-7) M VIP generated dose-related sphincter of Oddi relaxation, which was unaffected by atropine, propranolol, and phentolamine. The effect of CCK-8 was antagonized by dibutyryl cGMP (Bt2 cGMP) (10(-3) M), the VIP-antagonist (N-Ac-Tyr1, D-Phe2)-growth hormone-releasing factor-(1-29)-NH2, and abolished by tetrodotoxin. In contrast, VIP's relaxing action was tetrodotoxin insensitive. 10(-11)-10(-7) M CCK-8 stimulated dose-dependent release of VIP (0.5-2.2 fm/ml.mg tissue), which was not inhibited by atropine, propranolol, and phentolamine, but was antagonized by 10(-3) M Bt2 cGMP and tetrodotoxin. In addition CCK-8 and VIP generated dose-related (10(-10)-10(-7) M) increases in sphincter of Oddi cAMP levels that were not affected by atropine, propranolol, and phentolamine. Furthermore, 10(-5)-10(-2) M 8-bromo-cAMP caused dose-dependent relaxation of the sphincter of Oddi. In separate studies, a 2-h incubation in physiological solution containing 12 parts/1,000 of rabbit VIP antiserum antagonized sphincter relaxation caused by 4 nM CCK-8 and 6 nM VIP. The antiserum also significantly decreased the sphincter of Oddi cAMP level stimulated by 4 nM CCK-8 by 48 +/- 15%. These studies demonstrate that CCK-8 relaxes the canine sphincter of Oddi via a noncholinergic, nonadrenergic neural pathway involving VIP. The intracellular mechanism mediating CCK/VIP relaxation involves generation of cAMP.

Neural control of the sphincter of Oddi. A physiological role of 5-hydroxytryptamine in the regulation of basal sphincter of Oddi motor activity in the cat.

The effect of 5-hydroxytryptamine (5-HT) on the sphincter of Oddi (SO) was studied in the cat. The SO had two motor responses to 5-HT: the most common was an initial contraction followed by a more prolonged relaxation, and the other was an exclusive relaxation. Tetrodotoxin did not impair the magnitude of the net contraction induced by 5-HT, but it completely blocked the relaxation. Methysergide partially inhibited the SO contraction in response to submaximal doses of 5-HT (5-20 micrograms/kg). Atropine decreased the SO excitatory response to all doses of 5-HT. The combination of atropine and methysergide completely antagonized the 5-HT excitatory effect, which changed the SO biphasic response to an exclusive relaxation. After tetrodotoxin, the effect of 5-HT was almost completely antagonized by methysergide alone. The SO contraction and relaxation caused by 5-HT were almost completely blocked by 5-HT tachyphylaxis. In contrast, a 5-HT depletion with reserpine enhanced the sensitivity of the SO to 5-HT, responding to doses a thousand times smaller than in control animals. Hexamethonium, phentolamine, propranolol, and 5-methoxy-N,N-dimethyltryptamine did not antagonize the 5-HT-induced contraction or relaxation. These findings indicate that 5-HT caused SO contraction by stimulating postganglionic cholinergic neurons and the smooth muscle directly and caused relaxation by stimulating postganglionic, noncholinergic, nonadrenergic inhibitory neurons. 5-HT blockade or depletion resulted in a significant reduction in basal tonic pressures and in the amplitude of phasic contractions, which suggested that serotonergic neurons may play a physiologic role in the regulation of basal SO motor activity.

The human sphincter of Oddi. Physiology and pathophysiology.

The sphincter of Oddi (SO) is critically located at the junction of the common bile duct (CBD), main pancreatic duct, and the duodenum. It is a high-pressure zone with phasic contractions that regulate bile and pancreatic juice flow. The SO is probably regulated by several gastrointestinal hormones, and its basal pressure and phasic contractions can be elevated or decreased significantly by exogenous drugs. Its role in gallstone formation is probably negligible, but severing the SO allows one to extract CBD stones with an endoscope. Abnormal function of the SO can cause biliarylike pain. Of patients with persistent pain after cholecystectomy, 14% have abnormal SO manometric findings. Endoscopic or surgical sphincterotomy can cure these patients of their pain. The SO may play a significant role in the development of pancreatitis in certain patients, either because of the relationship of the CBD orifice to the pancreatic duct orifice created by the SO or because of the response of the SO to exogenous agents, such as alcohol.

Histomorphologic and molecular phenotypes predict gemcitabine response and overall survival in adenocarcinoma of the ampulla of Vater.

BACKGROUND: The need for adjuvant chemotherapy after resection of ampullary cancer (PapCa) remains undefined. Recent data suggest that a different epithelial origin of PapCa might be associated with different tumor biology. The aim of the present study was to assess the clinical value of morphologic and immunohistochemic subclassification of PapCa into intestinal-type (IT) and pancreaticobiliary-type (PT) to predict chemotherapy response and overall survival (OS). METHODS: Via a prospective database, 112 PapCa were identified, of which 95 could be included in the present study. Those were compared with 206 matching patients with periampullary pancreatic cancer (ie, pancreatic ductal adenocarcinoma, PDAC). IT and PT PapCa were classified morphologically, and tissue microarray was prepared with immunohistochemistry for CK7, CK20, MUC2, CDX2, ß-Catenin, and Villin. Multivariate survival analysis was performed. RESULTS: OS of PT patients was less compared with IT patients (25 vs 98 months; P < .001), whereas it was comparable with patients with PDAC (25 vs 14 months; P = .123). PT patients receiving adjuvant gemcitabine chemotherapy featured improved OS (32 vs 13 months; P = .013), whereas gemcitabine tended to be associated with decreased OS in IT patients (35 vs 112 months; P = .193). Besides histopathologic classification, expression of CK7 and MUC2 were important prognostic variables. PT patients with CK7-positivity or MUC2-negativity were segregated into an even poorer prognostic group. CONCLUSION: PapCa is not a separate tumor entity. We demonstrate important differences between IT-PapCa and PT-PapCa not only in long-term survival but also in response to adjuvant gemcitabine. Tumor biology and clinical course of PT tumors resemble those of PDAC. PT tumors should therefore be treated like PDAC.

Graded effect of protein on regional myoelectric activity of the opossum sphincter of Oddi.

Although it is known that the sphincter of Oddi exhibits a myoelectric response to intraluminal nutrients, the effect of specific dietary components has not been well characterized. The aim of this study was to determine the effect of intragastric instillation of a protein meal on regional myoelectric activity of the opossum sphincter of Oddi. Seven adult opossums were chronically prepared with self-retaining bipolar electrodes secured to the proximal and distal parts of the sphincter. After a 2-week recovery period, and with the animals fasted and conscious, myoelectric activity was recorded for two cycles of the migrating myoelectric complex. The animals then received graded calories of protein through an orogastric tube and recordings were continued until return of the fasted cyclic activity. Doses of 60, 120, and 240 kcal of protein elicited increases in myoelectric spike activity of the proximal sphincter of 18.7%, 41.9%, and 66.6%, respectively. Similarly, the length of the fed state was prolonged by increasing caloric loads, with mean (plus or minus standard error of the mean) times of 266 +/- 25, 292 +/- 15, and 375 +/- 42 minutes for each dose. A similar relationship was noted in the distal part of the sphincter. Regression analysis between the proximal and distal parts of the sphincter during the fasted and fed states showed a strong and persistent correlation of gradient of spikeburst frequency. We conclude that myoelectric spike frequency of the opossum sphincter of Oddi exhibits a dose-related response to intragastric protein calories. Furthermore, the proximal and distal parts of the sphincter remain electrically coupled, with the proximal region pacing the distal region during the fasted state and after protein administration.

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

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

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

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

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

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

Cholecystectomy alters the hormonal response of the sphincter of Oddi.

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

Effects of gastrointestinal hormones on Oddi's sphincter and duodenal myoelectric activity and pancreatobiliary pressure. Studies in the opossum.

Myoelectric activity of Oddi's sphincter and duodenum was correlated with common duct and pancreatic duct pressures in conscious opossums after infusion of the following substances: cholecystokinin, pentagastrin, glucagon, secretin, and acetylcholine. Cholecystokinin and pentagastrin increased and glucagon and secretin decreased the frequency of spike potentials in Oddi's sphincter and the duodenum. Acetylcholine was associated with the largest increase in spike potentials in both Oddi's sphincter and the duodenum. Although there was variation in the number of pressure elevations related to Oddi's sphincter spike potentials, the baseline pressure remained constant during administration of the hormones. Acetylcholine infusion increased the biliary and pancreatic pressures to 29 and 31 mm Hg, respectively. We conclude that gastrointestinal hormones may have an important role in regulating the excretion of bile and pancreatic juice into the duodenum.

Action of gastrointestinal hormones on the myoelectric activity of the sphincter of Oddi in living rabbit.

The aim of this work was to compare the action of gastrointestinal (GI) hormones on the myoelectrical activity of the sphincter of Oddi. Using an experimental design previously described, we studied the electrical activity of the sphincter of Oddi and compared the percentage variation in the number of spikes before and after injection of hormones. Increasing doses of the following hormones were injected i.v. at random: CCK, OP-CCK, caerulein, bombesin, gastrin, secretin and glucagon. CCK and caerulein (as previously found), and also bombesin, OP-CCK and gastrin increased the spikes activity of the sphincter of Oddi. Secretin had no effect and glucagon decreased this activity. There was no tachyphylaxis, but a good dose-effect relationship for each hormone. Compared on a molar basis caerulein is 8 times more effective than CCK and OP-CCK which in turn are more potent than bombesin. Gastrin acts only at pharmacological doses.

Effects of sphincterectomy on bile acid enterohepatic circulation in dogs.

Relative rates of bile enterohepatic circulation (EHC) and bile acid pool distribution were compared in intact and sphincterectomized dogs with portacaval shunt. There was no significant difference in the rates of EHC or in the bile acid pool distribution in the groups of animals. Feeding and cholecystokinin administration caused similar increases in bile acid EHC rates in sphincterectomized and intact animals. It was concluded that the sphincter of Oddi has little or no effect on these aspects of bile acid metabolism in dogs.

Gastrosphincter of Oddi reflex.

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

Effects of caloric stimuli on frog ampullar receptors.

The observation that caloric nystagmus can be evoked even in microgravity conditions argues against Barany's convective theory. To justify this result, gravity-independent mechanisms (mainly endolymphatic volume changes and direct action of the temperature on vestibular sensors) are believed to contribute to caloric-induced activation of vestibular receptors. To define the importance of both gravity-dependent and gravity-independent mechanisms, the posterior semicircular canal of the frog was thermally stimulated by a microthermistor positioned close to the sensory organ. The stimulus produced a gravity-dependent transcupular pressure difference that, depending on the position of the heater, could result in either excitation or inhibition of ampullar receptor sensory discharge. When the heater was positioned on the ampulla, or when the canal rested on the horizontal plane, no responses could be evoked by thermal stimuli. These results suggest that, in our experimental conditions (DeltaT up to 1.5 degrees C), neither a thermally induced expansion of the endolymph nor a direct action of the temperature on vestibular sensors play any major role.

Endoscopic electromyography and manometry of the human sphincter of Oddi.

The myoelectric and manometric activities of the sphincter of Oddi were recorded in 8 patients using an original probe passed through the papilla of Vater during duodenoscopy. The sphincter of Oddi's myoelectric activity showed rhythmic bursts of action potentials which appeared in correspondence with the ascending phase of the phasic pressure waves. On the basis of these results, we believe that electromyography could in some cases replace manometry for studying sphincter of Oddi motility, since it avoids pressure perfusion of the bilio-pancreatic tract, with its concomitant risks, and provides sufficient information for motor studies.

Conduction of activity between muscles in the terminal region of the common bile duct and in the neighboring duodenum.

The relationship between muscle activity at the terminal region of the common bile duct and the duodenal muscle was examined in rabbits. The rhythmic muscle activity in the terminal region was synchronous with duodenal muscle activity. The activity of the latter muscle preceded the former. The activity at the terminal region synchronous with the rhythmic activity of the duodenal muscle sometimes disappeared spontaneously. The muscle activity of the ampulla and the spincter at the terminal region was sometimes independently lost. The conduction of excitation from the duodenal muscle to the terminal region appeared to be performed at several sites. The existence of a "conduction-shunt path" between the terminal region and the duodenum, as well as between the ampulla and the sphincter appeared probably. Some quantitative differences were found between the spincter, ampulla and duodenum in inhibitory effects to stimulation of splanchnic nerves and reflex effects and to excitatory effects of cholecystokinin-pancreoxymin and caerulein. These results seem to indicate that the sympathetic nerves and the intramural cholinergic neurones controlling these region carry out activities quantitatively different from each other.

[Effect of physiological stimuli on Oddi's sphincter motility]. / Efeito de estímulos fisiológicos sobre a motricidade do esfíncter de Oddi.

The myoelectric activity of the sphincter of Oddi was studied both in the fasted and fed states and following administration of gastrointestinal hormones. Electromyographic recordings were obtained from 21 opossums in the fasted state and following administration of 20 Cal/kg of fat, protein, carbohydrate or isocaloric mixture of these three aliments. The proximal segment of the sphincter of Oddi generated spontaneous spike potentials that migrated to the distal segment of the sphincter. The frequency of spike potentials correlated with the migrating myoelectric complex in the duodenum. Following feeding, the migrating myoelectric complex was abolished and substituted by a fed pattern. The duration of the fed pattern and the frequency of spike potentials depended on the kind of aliment. Cholecystokinin and pentagastrin increased and glucagon and secretion decreased the frequency of spike potentials in the sphincter of Oddi. It is concluded from these studies that the sphincter of Oddi may play an important role in controlling the time and rate of biliary drainage into the duodenum.

[Postoperative functional evaluation and pharmacological study of Oddi's sphincter by means of cholangiomanometry using a Kehr tube]. / Valutazione funzionale post-operatoria e studio farmacologico dell'Oddi mediante colangiomanometria trans-Kehr.

The Authors report their experience of postoperative cholangiomanometry carried out through a T-tube on 19 patients; in 13 of such patients the Oddi's sphincter was intact, while 6 of them underwent sphincterectomy. In 8 patient's a manometric study of the duodenum was associated. They performed both variable flow and pressure and constant flow manometry and their results show that such examination is a reliable test both for the functional evaluation of the surgical procedure, and for the study of the action of various drugs on Oddi's sphincter function and its correlation with duodenal motility.