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PubMed1981

Periodic contractions of the canine gallbladder during the interdigestive state.

Interdigestive contractile activity of the gallbladder, the stomach, and the duodenum was measured by means of chronically implanted force transducers in five conscious dogs. During the interdigestive state, contractions of the gallbladder were identified to be closely associated with the initial period of phase II of the interdigestive migrating contractions (IMC) in the duodenum. The mean contractile force of the gallbladder during this phase was 6.5 +/- 0.77 g, which corresponded to approximately 80% of the force of the postprandial contractions. When the duodenum exhibited phase II contractions, the gallbladder had already returned to the resting level. Intravenous infusion of synthetic motilin induced IMC in the stomach and duodenum and during the initial period of motor response of the duodenum reproduced contractions in the gallbladder that were identical to the natural contractions as to their period and pattern. We cannot yet ascribe the interdigestive contractions observed in the gallbladder to the direct action of motilin, but the present study clearly indicates that the gallbladder contracts even in the interdigestive state, and the contractions are associated with the phase II contractions in the duodenum.

Animals↗

PubMed1986

Gallbladder prostaglandins and lysophospholipids as mediators of mucin secretion during cholelithiasis.

Mucin hypersecretion from the gallbladder epithelium contributes to cholesterol gallstone formation by accelerating the nucleation of cholesterol-supersaturated bile. Prostaglandins (PGs) and lysophosphatidylcholine (LPC) have both been implicated as potential mediators of mucin hypersecretion, but their roles are unclear. We fed prairie dogs a lithogenic diet (0.34% cholesterol), and after 1, 2, 4, or 6 wk of cholesterol feeding, we measured glycoprotein and LPC concentrations in bile and PG synthesis in gallbladder and liver slices. Hypercholesterolemia and cholesterol supersaturation of bile occurred after 1 wk of cholesterol feeding, but marked crystal formation was delayed until 4 wk, when glycoprotein concentrations became markedly elevated. Glycoprotein hypersecretion was preceded by increased synthesis of PGF2 alpha (P less than 0.002), PGE2 (P less than 0.001), prostacyclin (P less than 0.05), and thromboxane (P = 0.07) in the gallbladder after only 2 wk of cholesterol feeding, but PG synthesis in the liver remained unchanged (P greater than 0.14). LPC concentrations in gallbladder bile also increased at 2 wk (P less than 0.02), but LPC in hepatic bile was unchanged (P = 0.35). In organ culture studies, LPC caused a dose-dependent stimulation of [3H]glycoprotein release from guinea pig gallbladder mucosa that could not be explained solely by LPC's detergent properties. We conclude that gallbladder PG synthesis and LPC production are increased at an early stage of cholesterol gallstone formation in the prairie dog model. These changes probably play a significant role in gallstone pathogenesis, since they mediate hypersecretion of gallbladder mucin and thus favor the nucleation of cholesterol-supersaturated bile.

Animals↗

PubMed1995

Bile salt-dependent inhibition of gallbladder emptying.

Little is known about the inhibitory controls of gallbladder emptying. Since cholestyramine, a binding agent that reduces luminal concentration of bile salt, has been reported to accelerate gallbladder emptying, suggesting that bile salt is inhibitory, we hypothesized that fat-stimulated gallbladder emptying is inhibited by a bile salt-dependent mechanism. To test this idea, we compared gallbladder emptying in 10 dogs equipped with duodenal and jejunal fistulas that allowed for complete diversion of the native bile while varying concentrations of bile salt were perfused into the small intestine. In six dogs, 30 mM oleate and 5, 10, or 20 mM sodium taurocholate was perfused into the whole intestine. Since bile salt availability alters fat absorption, in a separate experiment in seven dogs we also compared gallbladder emptying while 30 mM oleate and 5 mM taurocholate were perfused between fistula and 0, 5, 10, or 20 mM taurocholate were perfused beyond jejunal fistula to separate fat from varying concentrations of bile salt. We found that intestinal taurocholate inhibited fat-stimulated gallbladder emptying in a dose-dependent fashion (P < 0.01; analysis of variance, significant linear dose effect) and that the inhibitory effect of bile salt persisted when 5-20 mM taurocholate was perfused beyond the jejunal fistula (0 vs. average of 5-20 mM taurocholate, P < 0.05, paired t-test). We conclude that fat-stimulated gallbladder emptying is inhibited by a bile salt-dependent inhibitory mechanism.

Anastomosis, Surgical↗

PubMed1998

Impaired G protein function in gallbladder muscle from progesterone-treated guinea pigs.

This study was designed to elucidate the mechanism of action of progesterone on gallbladder smooth muscle in guinea pigs. Adult male guinea pigs were treated with either progesterone (2 mg.kg-1.day-1) or saline for 7 days. Gallbladder muscle cells were isolated by enzymatic digestion with collagenase. Contractile responses to agonists were expressed as percent shortening from control cell length. [35S]guanosine 5'-O-(3-thiotriphosphate) ([35S]GTP gamma S)-binding properties of G proteins were assessed in crude membranes of gallbladder muscle with or without cholecystokinin octapeptide (CCK-8) stimulation. Gallbladder muscle cells from progesterone-treated guinea pigs exhibited an impaired contractile response to CCK-8, GTP gamma S, or aluminum fluoride but a normal response to potassium chloride or D-myo-inositol 1,4,5-trisphosphate compared with controls. Western blot analysis of gallbladder muscle revealed the presence of Gi1-2, Gi3, Gq/11, and Gs proteins. The maximal contraction induced by CCK-8 was blocked by pertussis toxin and Gi alpha 3-specific antibodies, but not by Gi alpha 1-2 or Gq/11 alpha antibodies. CCK-8 caused a significant increase in [35S]GTP gamma S binding to Gi alpha 3, but not to Gq/11 alpha or Gi alpha 1-2. The stimulation of Gi alpha 3 binding, however, was significantly reduced in gallbladder muscle membranes from progesterone-treated guinea pigs compared with that in control animals. In conclusion, progesterone might cause gallbladder hypomotility by downregulating Gi3 proteins.

Aluminum Compounds↗

PubMed1999

CCK receptor dysfunction in muscle membranes from human gallbladders with cholesterol stones.

Human gallbladders with cholesterol stones exhibit impaired muscle contraction induced by agonists that act on transmembrane receptors, increased membrane cholesterol content, and abnormal cholesterol-to-phospholipid ratio compared with those with pigment stones. The present study was designed to investigate the functions of the CCK receptor of gallbladder muscle membranes by radioreceptor assay and cross-linking. 125I-labeled CCK-8 binding was time-dependent, competitive, and specific. Scatchard analysis showed that the maximum specific binding (Bmax) was significantly decreased in cholesterol compared with pigment stone gallbladders (0.18 +/- 0. 07 vs. 0.38 +/- 0.05 pmol/mg protein, P < 0.05). In contrast, the affinity for CCK was higher in cholesterol than pigment stone gallbladders (0.18 +/- 0.06 vs. 1.2 +/- 0.23 nM). Similar results were observed in binding studies with the CCK-A receptor antagonist [3H]L-364,718. Cross-linking and saturation binding studies also showed significantly less CCK binding in gallbladders with cholesterol stones. These abnormalities were reversible after incubation with cholesterol-free liposomes. The Bmax increased (P < 0.01) and the dissociation constant decreased (P < 0.001) after incubation with cholesterol-free liposomes. In conclusion, human gallbladders with cholesterol stones have impaired CCK receptor binding compared with those with pigment stones. These changes are reversed by removal of the excess membrane cholesterol. These receptor alterations may contribute to the defective contractility of the gallbladder muscle in patients with cholesterol stones.

Bile Pigments↗

PubMed1976

Interaction of gastrin I, secretin, and cholecystokinin on gallbladder smooth muscle.

The effect of cholecystokinin (CCK), the octapeptide of cholecystokinin (CCK-OP), gastrin I, and secretin was studied on guinea pig gallbladder smooth muscle in vitro. Both CCK and CCK-OP stimulated gallbladder contraction, with CCK-OP being more potent. Gastrin I, over a wide dose range, had no effect on gallbladder contractility. Secretin alone also showed no effect on gallbladder smooth muscle but in combination with CCK-OP it produced a noncompetitive type of inhibition. Michaelis-Menten kinetics showed the calculated maximum response of the secretin plus CCK-OP interaction to be less than with CCK-OP alone. There was no change in the dose required to achieve half-maximal response, D50. These studies indicate that: a) CCK-OP has a greater effect on gallbladder contractility than CCK, b) gastrin I has no effect on gallbladder muscle tone, and c) secretin acts as a noncompetitive antagonist of CCK-OP. These findings suggest that gallbladder motor function may be determined in part by the interaction of secretin and CCK rather than solely in response to CCK.

Animals↗

PubMed2002

Endoscopic ultrasound-guided gallbladder bile aspiration in idiopathic pancreatitis carries a significant risk of bile peritonitis.

BACKGROUND: Direct microscopic examination of bile for the presence of microlithiasis is often performed during the evaluation of patients with idiopathic pancreatitis. Bile sampled from the duodenum and/or the common bile duct may not represent gallbladder bile, and thus may be inadequate for the diagnosis of microlithiasis. AIM: We sought to determine the safety and efficacy of endoscopic ultrasound (EUS)-guided fine-needle aspiration (FNA) of gallbladder bile in patients with idiopathic pancreatitis. METHODS: Patients with idiopathic pancreatitis underwent EUS with a linear echoendoscope. After excluding potential causes of pancreatitis such as common bile duct stones or pancreatic lesions, the gallbladder was identified. The gallbladder lumen was entered using a 22-gauge FNA needle via the duodenal wall. Bile was aspirated and analyzed for the presence of cholesterol monohydrate crystal, calcium bilirubinate granules, calcium carbonate microspheroliths and mucin gel strands. RESULTS: Three patients underwent EUS-guided FNA of gallbladder bile. Two of these patients developed bile peritonitis within one hour of the procedure prompting us to discontinue the study. One patient's gallbladder bile contained microlithiasis. This patient had bile aspirated from the common bile duct via ERCP 3 weeks prior to EUS. However, analysis of that bile sample failed to show microlithiasis. CONCLUSION: Unfortunately, transduodenal EUS-guided FNA of gallbladder bile using a 22-gauge needle carries a significant risk of bile peritonitis.

Acute Disease↗

PubMed2002

Active relaxation of human gallbladder muscle is mediated by ATP-sensitive potassium channels.

BACKGROUND: Active and significant relaxation of the human gallbladder must be one of the facets of its motility during both the filling and emptying cycle. Conflicting reports about the presence or significance of nitric oxide have been reported in the literature. The aim of this study was to investigate the role of nitric oxide and K(ATP) channels in human gallbladder muscle using isolated strips from human gallbladder. METHODS: Full thickness strips were obtained from 56 human gallbladders and suspended under isometric tension in organ baths. The effect of nitric oxide donors and inhibitors on cholecystokinin octapeptide- and carbachol-induced contraction was examined. In separate experiments the effect of the K(ATP) channel activator, cromakalim, and the inhibitor, glibenclamide, were determined. RESULTS: Cromakalim induced a significant relaxation of agonist-induced contraction in human gallbladder in vitro, an effect which was abolished by the K(ATP) channel inhibitor glibenclamide. No evidence of significant nitric oxide involvement in relaxation was observed. CONCLUSIONS: This study has demonstrated the presence of K(ATP) channels in human gallbladder for the first time. These are capable of causing significant relaxation in the presence of hormonal and muscarinic agonists and may represent a major pathway for gallbladder relaxation.

Adenosine Triphosphate↗

PubMed1981

Effect of a lithogenic diet on cell proliferation in the murine gallbladder epithelium.

A cholesterol-cholic acid lithogenic diet was administered to mice for periods from 2 days to 12 weeks. Intraperitoneal injections of tritiated thymidine and autoradiographs were used for the estimation of the proliferative parameters in the gallbladder epithelium. The total DNA content of the gallbladder was determined. Significantly higher labeling (p less than 0.01) and mitotic (p less than 0.01) indices were observed from the 2nd day and the total DNA content of the gallbladder was increased (p less than 0.01) from the 2nd week of the diet. Increased proliferative activity was followed by hyperplasia of the gallbladder epithelium. A significant dilatation of the gallbladders was also noted from the 2nd day of the diet (p less than 0.01). Gallstones appeared after at least 4 weeks. Our results indicate that gallstone formation is preceded by a higher proliferative activity in the gallbladder mucosa. Distension of the gallbladder could be one of the factors explaining this phenomenon in mice, but the influence of intraluminal modifications in the bile salt composition cannot be excluded.

Animals↗

PubMed1988

Gallbladder emptying in duodenal ulcer patients having undergone Billroth II gastrectomy.

There is an increased incidence of gallstones in patients who have undergone Billroth II (BII) gastrectomy for duodenal ulcer. To explore the mechanisms underlying this, we examined changes in gallbladder volume induced by a meal and by intravenous administration of cerulein, in 13 BII patients and in 13 normal subjects. Gallbladder volume was measured by real-time ultrasonography. In the fasting state, gallbladder volumes were significantly larger in BII patients than in controls. The percent decrease in gallbladder volume after the meal was significantly less and maximum volume reduction observed throughout the study occurred sooner in BII patients than in controls. In contrast, the kinetics and magnitude of the reduction in gallbladder volume induced by cerulein were similar in the two groups. These findings suggest that the altered gallbladder response to a meal is due to impaired postprandial stimulation of gallbladder following BII gastrojejunostomy.

Adult↗

PubMedDate not supplied

Fine needle aspiration cytodiagnosis of primary squamous cell carcinoma of the gallbladder. Report of two cases.

BACKGROUND: Cytologic descriptions of the diagnosis of the rare primary carcinoma of the gallbladder are sparse. The obstacles to the diagnosis are ascribed to vague symptoms and inaccessibility of the gallbladder to biopsy. We describe two cases of primary squamous cell carcinoma of the gallbladder that were diagnosed using fine needle aspiration (FNA) cytology. CASES: Both patients were elderly females with vague symptoms of abdominal pain, jaundice, loss of weight, anorexia and mild fever. Imaging studies showed enlargement of the gallbladder with a soft tissue mass in the fundus and abnormally thickened wall, indicative of a tumor. Also, in case 1, gallstones and enlarged, matted paraaortic and porta hepatis lymph nodes were present. FNA of the gallbladder was done after selection of a suitable puncture site and needle positioning, which was confirmed by computed tomography. The aspirated material was collected as needle and syringe washings, and from half the material filter preparations were made and stained for cytologic study, while the remainder was used for making cell blocks for histologic study. Both cases showed cytohistologic features of a moderately well differentiated, necrotizing squamous cell carcinoma characterized by keratinizing malignant cells with orangeophilic cytoplasm. In both cases immunostaining for high-molecular-weight keratins (AE1/AE3) and cytokeratin (CAM 5.2) was positive, while staining for carcinoembryonic antigen, B72.3 and other markers was negative. CONCLUSION: This study further confirmed that with the widespread use of more-sophisticated imaging techniques, the gallbladder is becoming more readily accessible to visualization. In view of this, FNA cytodiagnosis holds promise as a noninvasive technique in the diagnosis of gallbladder neoplasms.

Aged↗

PubMed1976

Regulation of pancreatic and gallbladder functions by intraluminal fatty acids and bile acids in man.

The effects of intraduodenal glycerol, fatty acid (FA) chain length and FA loads, and bile acid (BA) concentrations on pancreatic and gallbladder function were investigated in 31 healthy volunteers by a perfusion method. FA absorption rates in the duodenum and proximal jejunum were measured simultaneously. Pancreatic and gallbladder responses were augmented by increasing FA chain length and FA loads until the "maximal" secretory capacity of the pancreas and gallbladder emptying was attained. Glycerol had no effect. Raising BA concentrations above the critical micellar concentration accelerated FA absorption rates but decreased the magnitude of pancreatic and gallbladder responses to FA. Higher BA concentrations exerted an opposite effect, slowing FA absorption and increasing pancreatic and gallbladder responses. Indeed, a significant, inverse correlation was found between FA absorption and pancreatic and gallbladder responses to FA, suggesting a relationship between the length of intestine exposed to FA and the amount of cholecystokinin (and/or other neurohormonal factors) released, which stimulates pancreatic secretion and gallbladder contraction.

Adult↗

PubMed1980

Effect of cholecystokinin and the octapeptide of cholecystokinin on the feline sphincter of Oddi and gallbladder. Mechanisms of action.

We studied the effect of cholecystokinin (CCK) and the octapeptide of cholecystokinin (OP-CCK) on the feline gallbladder and sphinecter of Oddi. Both CCK caused a dose-dependent gallbladder contraction and sphincter of Oddi relaxation. The half-maximal responses of the sphincter of Oddi were 6 ng/kg for OP-CCK and 0.15 Ivy-dog U/kg for CCK, which were lower than those of the gallbladder with 28 ng/kg and 0.32 Ivy-dog U/kg, respectively. The effect of OP-CCK on the gallbladder was partially blocked by tetrodotoxin (P < 0.02), hexamethonium alone (P < 0.05), or a combination of hexamethonium and atropine (P < 0.01). The gallbladder response to CCK was not blocked by either atropine alone (P < 0.60) or adrenergic antagonists (P > 0.40). The sphincter of Oddi response to OP-CCK was blocked by tetrodotoxin (P < 0.001) but it was not blocked by cholinergic (P < 0.20) or adrenergic antagonists (P < 0.60). After complete denervation with tetrodotoxin, OP-CCK caused sphincter of Oddi contraction. These findings indicate that there are two excitatory receptors for CCK in the gallbladder, one at the cholinergic neurons and the other at the level of the gallbladder muscle. There are also two receptors for CCK in the sphincter of Oddi, one that is inhibitory, and present at the noncholinergic, nonadrenergic neurons, and the other, excitatory, at the circular muscle.

Ampulla of Vater↗

PubMed1989

Effects of a novel cholecystokinin (CCK) receptor antagonist, MK-329, on gallbladder contraction and gastric emptying in humans. Implications for the physiology of CCK.

To explore the physiology of cholecystokinin (CCK) in humans, we investigated the effect on gallbladder contraction and gastric emptying of a recently developed CCK receptor antagonist, MK-329. In a double-blind, four-period crossover study eight subjects received single doses of 0.5, 2, or 10 mg MK-329, or placebo, followed by an intravenous infusion of CCK-8 (30 pmol/kg.h). In placebo-treated subjects gallbladder volumes decreased on average to 43% of initial volumes after 2 h of CCK infusion. MK-329 caused a dose-dependent inhibition of CCK-stimulated gallbladder contraction with 10 mg producing complete blockade (P less than 0.01, cf. placebo). Gallbladder contraction and gastric emptying rates after a mixed meal were then measured in a two-period crossover study. Subjects received placebo or 10 mg of MK-329 2 h before eating. Gastric emptying of both solids and liquids was measured simultaneously by gamma scintigraphy. In placebo-treated subjects plasma CCK levels increased postprandially to 2.3 pM, gallbladder volumes decreased 68.4 +/- 3.8% (SE), and the times for 50% emptying of liquids and solids from the stomach were 58 +/- 10 and 128 +/- 8 min, respectively. In MK-329-treated subjects there was a marked elevation in peak CCK levels to 13.8 pM (P less than 0.01, cf. placebo), and gallbladder contraction was completely inhibited. Solid and liquid emptying rates were unaffected. These findings demonstrate that (a) MK-329 is a potent, orally active antagonist of CCK in humans, and (b) CCK is the major regulator of postprandial gallbladder contraction. These data also support the concept of negative feedback regulation of CCK secretion and suggest that mechanisms other than CCK play a dominant role in the regulation of postprandial gastric emptying rates.

Adult↗

PubMed2002

Expression of cytokine and chemokine mRNA and secretion of tumor necrosis factor-alpha by gallbladder epithelial cells: response to bacterial lipopolysaccharides.

BACKGROUND: In addition to immune cells, many other cell types are known to produce cytokines. Cultured normal mouse gallbladder epithelial cells, used as a model system for gallbladder epithelium, were examined for their ability to express the mRNA of various cytokines and chemokines in response to bacterial lipopolysaccharide. The synthesis and secretion of the tumor necrosis factor-alpha (TNF-alpha) protein by these cells was also measured. RESULTS: Untreated mouse gallbladder cells expressed mRNA for TNF-alpha, RANTES, and macrophage inflammatory protein-2 (MIP-2). Upon treatment with lipopolysaccharide, these cells now produced mRNA for Interleukin-1beta (IL-1beta), IL-6, monocyte chemoattractant protein-1 (MCP-1), and showed increased expression of TNF-alpha and MIP-2 mRNA. Untreated mouse gallbladder cells did not synthesize TNF-alpha protein; however, they did synthesize and secrete TNF-alpha upon treatment with lipopolysaccharide. METHODS: Cells were treated with lipopolysaccharides from 3 strains of bacteria. Qualitative and semi-quantitative RT-PCR, using cytokine or chemokine-specific primers, was used to measure mRNA levels of TNFalpha, IL-1beta, IL-6, IL-10, KC, RANTES, MCP-1, and MIP-2. TNF-alpha protein was measured by immunoassays. CONCLUSION: This research demonstrates that gallbladder epithelial cells in response to lipopolysaccharide exposure can alter their cytokine and chemokine RNA expression pattern and can synthesize and secrete TNFalpha protein. This suggests a mechanism whereby gallbladder epithelial cells in vivo may mediate gallbladder secretory function, inflammation and diseases in an autocrine/paracrine fashion by producing and secreting cytokines and/or chemokines during sepsis.

Animals↗

PubMed2004

Megalin and cubilin expression in gallbladder epithelium and regulation by bile acids.

Cholesterol crystal formation in the gallbladder is a key step in gallstone pathogenesis. Gallbladder epithelial cells might prevent luminal gallstone formation through a poorly understood cholesterol absorption process. Genetic studies in mice have highlighted potential gallstone susceptibility alleles, Lith genes, which include the gene for megalin. Megalin, in conjunction with the large peripheral membrane protein cubilin, mediates the endocytosis of numerous ligands, including HDL/apolipoprotein A-I (apoA-I). Although the bile contains apoA-I and several cholesterol-binding megalin ligands, the expression of megalin and cubilin in the gallbladder has not been investigated. Here, we show that both proteins are expressed by human and mouse gallbladder epithelia. In vitro studies using a megalin-expressing cell line showed that lithocholic acid strongly inhibits and cholic and chenodeoxycholic acids increase megalin expression. The effects of bile acids (BAs) were also demonstrated in vivo, analyzing gallbladder levels of megalin and cubilin from mice fed with different BAs. The BA effects could be mediated by the farnesoid X receptor, expressed in the gallbladder. Megalin protein was also strongly increased after feeding a lithogenic diet. These results indicate a physiological role for megalin and cubilin in the gallbladder and provide support for a role for megalin in gallstone pathogenesis.

Animals↗

PubMed1990

Gallbladder wall thickening (congestive cholecystopathy) in chronic liver disease: a sign of portal hypertension.

A thickened gallbladder wall is often seen with ultrasound in alcoholic cirrhosis. Hypoalbuminaemia is thought to be the cause since there is a strong association between bowel wall thickening and low serum albumin. To determine the role of portal hypertension in producing gallbladder wall thickening we studied 40 consecutive stable patients-37 with cirrhosis and three with portal hypertension due to primary biliary cirrhosis. Ultrasound assessment of the gallbladder wall was made after an overnight fast using a Technicare autosector. Wall thickness 4 mm or greater was considered abnormal. Twenty-seven patients had a thickened gallbladder wall and all had evidence of portal hypertension. Hypoalbuminaemia was not an important factor since it was only present in six cases with thickened walls. In two cases reduction in portal pressure with oral propranolol was associated with a decrease in gallbladder wall thickness. These results suggest that portal hypertension, not hypoalbuminaemia, is the dominant factor causing gallbladder wall thickening in cirrhosis. Ultrasound demonstration of gallbladder wall thickening in chronic liver disease should suggest the presence of portal hypertension.

Chronic Disease↗

PubMed1993

Gallbladder function after endoscopic sphincterotomy--a dynamic ultrasound assessment.

There is controversy regarding the function of the gallbladder following endoscopic sphincterotomy (ES) for the treatment of gallstones. Using ultrasound to assess gallbladder volume, we evaluated gallbladder contractility in 34 patients (18 male, 16 female), mean age 73 years, who had ES and common bile duct (CBD) clearance a mean of 18 months earlier. In 16 patients gallbladder function could not be measured, either because the fasting gallbladder was small and contracted or because it contained gas. The remaining 18 patients (53%) had "normal" gallbladder contraction with a mean initial fasting volume of 30.3 ml and mean post fatty meal volume of 13.8 ml. 14 of these 18 patients had a repeat fasting volume which showed refilling in all except one. Those with a functioning gallbladder had had significantly smaller stones extracted from the CBD at the time of ES. A smaller or incomplete sphincterotomy may have been performed in these patients, therefore allowing some residual sphincter of Oddi function.

Adult↗