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PubMed1984

Human gallbladder mucin accelerates nucleation of cholesterol in artificial bile.

The gallbladder bile of patients with cholesterol gallstones is characterized by two abnormalities: (a) supersaturation with cholesterol and (b) accelerated nucleation of cholesterol monohydrate crystals. We studied the ability of purified human gallbladder mucin to nucleate artificial bile in vitro. Human gallbladder mucin at concentrations of 2 and 4 mg/ml accelerated the nucleation time of cholesterol crystals in model bile. The mean number of cholesterol crystals in artificial bile incubated for 10 days with 4 mg/ml of human gallbladder mucin was 2327/mm3 (p less than 0.01) vs. control of 51/mm3. The number of crystals found in model bile was dependent on the concentration of human gallbladder mucin (2-16 mg/ml) and the time of incubation (4-14 days). Human gallbladder mucin was associated with an increase in the number of liquid crystals after 4 days of incubation, which then decreased in number as solid cholesterol monohydrate crystals formed. Nucleation by human gallbladder mucin was significantly increased only with cholesterol saturation indices greater than 1.0, and in biles containing 10% but not 3% total lipid by weight. Pooled human gallbladder mucin from gallbladders with and without stones both increased nucleation significantly when compared with controls. Increased nucleation of saturated model bile was also observed with purified monkey cervical and bovine gallbladder mucin, but not with porcine gastric mucin. These observations provide further evidence that human gallbladder mucin may contribute to cholesterol gallstone formation in humans by accelerating nucleation of cholesterol monohydrate crystals from supersaturated gallbladder bile.

Animals↗

PubMed1984

Variations in concentrating function of the gallbladder in the conscious monkey.

Hepatic bile is concentrated in the gallbladder by absorption of water and electrolytes. The rate of water absorption can be influenced in vitro and in vivo by gastrointestinal hormones and neurogenic transmitters. Recent studies have demonstrated that besides its absorbing activity, the gallbladder has the ability to secrete fluid into its lumen. In the present experiments, we studied the rate of net water absorption in the gallbladders of pig-tailed monkeys sitting in restraining chairs. Bile from the common bile duct and the gallbladder was led out through cannulas to a stream splitter, samples were obtained, and bile was returned to the duodenum. By measuring outflow from the gallbladder and the concentration of bile acids in hepatic bile and bile that had passed through the gallbladder, net water absorption from the gallbladder bile could be calculated. The results demonstrate that during daytime fasting there was a net absorption corresponding to 30% of the fasting gallbladder volume per hour, and after feeding there was a net secretion of fluid into the gallbladder lumen. Compared with the awake fasting state, net water absorption from the gallbladder decreased at night while the animal was fasting and asleep. Physiologically, secretion of fluid after a meal could help to empty the gallbladder, and changes in net water absorption by the gallbladder could influence the kinetics of the enterohepatic circulation of bile acids.

Absorption↗

PubMed1983

Coordination of gastric and gallbladder emptying after ingestion of a regular meal.

The relationship of gallbladder emptying and refilling to gastric emptying of solids, gastrointestinal transit time, and human pancreatic polypeptide response was examined after ingestion of a standard breakfast (40% fat) in 12 healthy men and women. Gallbladder volume, emptying, and refilling was measured by real-time ultrasonography, and gastric emptying of solids was measured scintigraphically by the disappearance from the stomach of egg labeled with 99mTc-sulfur colloid. Gastrointestinal transit time was defined as the time of initial rise in breath hydrogen following ingestion of 10 g of lactulose. Serum human pancreatic polypeptide level was measured by radioimmunoassay. Gallbladder emptying was biphasic, initially 0.015 +/- 0.003 min-1 and later 0.005 +/- 0.001 min-1, and gallbladder volume remained small until refilling began at 249 +/- 67 min. Gallbladder refilling was 70% complete at 335 +/- 57 min. The slower rate of gallbladder emptying and tonic gallbladder contraction occurred during gastric emptying of solids. Gallbladder refilling began when approximately 13% of solids remained in the stomach. Serum human pancreatic polypeptide showed the expected biphasic response to the meal and returned to basal levels at approximately the time of initiation of gallbladder refilling. The gastrointestinal transit time of women was twice that of men (73.6 +/- 20.2 vs. 37.5 +/- 22.7, p = 0.025). No other sex-related differences were detected. We conclude that gastric emptying of the solid portion of a meal containing fat maintains tonic gallbladder contraction through continued release of humoral mediators from small bowel and pancreas. When gastric emptying nears completion, humoral stimulation ceases and the gallbladder refills. Human pancreatic polypeptide does not appear to be responsible for gallbladder refilling.

Adult↗

PubMed1993

Characterization of cholecystokinin receptors on the human gallbladder.

BACKGROUND: Several studies examined in vivo and in vitro biologic activity of the human gallbladder in response to cholecystokinin (CCK). However, few studies have demonstrated directly the interaction of CCK with receptors on the human gallbladder, which is responsible for this biologic activity. METHODS: To characterize CCK receptors on human gallbladder tissue, gallbladders were removed from human donor grafts that were being used for liver transplantation. The gallbladders were rapidly frozen and sectioned for measurement of binding of 125I-Bolton-Hunter-labeled-CCK-8 and were cut into strips for in vitro bioassay. RESULTS: Binding of 125I-BH-CCK-8 to human gallbladder was saturable, specific, and dependent on time, pH, and temperature. The binding was inhibited only by cholecystokinin-related peptides including CCK-8 (IC50 10 +/- 1.0 nmol/L) (mean +/- SD), des(SO3) CCK-8 (IC50 0.9 +/- 0.2 mumol/L), and gastrin-17-I (IC50 9.0 +/- 2.0 mumol/L) or specific CCK receptor antagonist L-364,718. Computer analysis of binding of 125I-BH-CCK-8 to gallbladder tissue showed a single class of binding sites with high affinity for CCK-8. Autoradiography localized binding of 125I-BH-CCK-8 only to the smooth muscle layer of the gallbladder. In the bioassay des(SO3) CCK-8 (EC50 1.2 +/- 0.7 mumol/L) and gastrin-17-I (EC50 4.5 +/- 2.4 mumol/L) were 150- and 563-fold less potent than CCK-8 (EC50 8.0 +/- 2.2 nmol/L). The relative potencies of CCK agonists for inhibiting binding of 125I-BH-CCK-8 agreed closely with their relative potencies for causing gallbladder contraction. The dose-response curve for CCK-8 alone to induce gallbladder contraction was not significantly different from those caused by CCK-8 plus 1 mumol/L tetrodotoxin or 1 mumol/L atropine. CONCLUSIONS: These results characterized the CCK receptors on smooth muscle of human gallbladder as sulfate dependent and causing gallbladder contraction.

Autoradiography↗

PubMed2002

Gallbladder contractility in patients with cirrhotic versus malignant ascites.

PURPOSE: The aim of this study was to evaluate differences in gallbladder contractility by measuring gallbladder wall thickness, fasting and residual gallbladder volume, and gallbladder ejection fraction in patients with cirrhotic and malignant ascites. METHODS: Twenty-four patients (16 women and 8 men) with malignant ascites (2 cervical, 2 colon, 2 stomach, 6 pancreatic, and 12 ovarian carcinomas), aged 59 +/- 12 years, and 26 patients (14 women and 12 men) with cirrhotic ascites, aged 57 +/- 16 years, were included in the study. After patients fasted overnight for 8 hours, gallbladder wall thickness, fasting gallbladder volume, and gallbladder volume and ejection fraction were measured sonographically at 10, 20, 30, 40, 50, 60, 70, 80, and 90 minutes after ingestion of a standard liquid test meal. RESULTS: The mean gallbladder wall thickness was higher in patients with cirrhotic ascites than in those with malignant ascites (5.5 +/- 1.5 mm [standard deviation] versus 3.1 +/- 0.6 mm, respectively; p < 0.001). The mean fasting gallbladder volume was also higher in patients with cirrhotic ascites than in those with malignant ascites (27.3 +/- 11.5 cm(3) versus 17.6 +/- 8.9 cm(3); p < 0.05). Patients with cirrhotic ascites had significantly higher mean postprandial gallbladder volumes and ejection fractions than did those with malignant ascites at all times except 10 minutes after the meal (p < 0.05). CONCLUSIONS: Our findings suggest that gallbladder contractility is greater in patients with cirrhotic ascites than in patients with malignant ascites.

Adult↗

PubMed1997

Precision of the gallbladder ejection fraction obtained with Tc-99m-pyridoxyl-5-methyl-tryptophan (99mTc-PMT) hepatobiliary scintigraphy as compared with the contraction ratio in three-dimensional computed tomography.

UNLABELLED: The gallbladder ejection fraction (GBEF) obtained with Tc-99m-pyridoxyl-5-methyl-tryptophan (99mTc-PMT) hepatobiliary scintigraphy has been used as a parameter of gallbladder function. To determine the accuracy of GBEF, the relationship with the contraction ratio of the gallbladder (GBCR) obtained with three-dimensional helical computed tomography (3D-CT) was studied. PATIENTS AND METHODS: A normal volunteer, 8 patients suffering from cholecystolithiasis and a patient with gallbladder dyskinesia were examined. The percent initial dose (%ID) for the gallbladder and GBEF with hepatobiliary scintigraphy were used to compare the volume of the gallbladder and GBCR which was measured by 3D-CT. RESULTS: The %ID of the gallbladder was correlated with the volume of the gallbladder by 3D-CT (Y = 1.000X - 1.818, r = 0.928). GBEF was correlated well with GBCR by 3D-CT (Y = 0.916X + 6.296, r = 0.975). CONCLUSIONS: The %ID of the gallbladder obtained with hepatobiliary scintigraphy may be a good indicator of the volume of the gallbladder. The accuracy of GBEF was confirmed by comparison with 3D-CT examination. GBEF is considered a useful parameter of pathophysiological gallbladder function.

Adult↗

PubMed1989

Stonebearing gallbladders: CT anatomy as the key to safe percutaneous lithotripsy. Work in progress.

Percutaneous cholecystolithotripsy can be performed with a transhepatic or transperitoneal approach. Because the anatomy of the gallbladder varies from person to person, the authors began a study to evaluate the position of the gallbladder with computed tomographic scans of 100 patients known to have stones in their gallbladders. Four variations in the relationship of the gallbladder to the liver and anterior abdominal wall were noted: completely intrahepatic gallbladders (39%) (type I), gallbladders bulging anterior to the anterior rim at least in part (35%) (type II), gallbladders completely anterior to the liver (17%) (type III), and gallbladders in a lateral position (9%) (type IV). In 51%, the colon was in direct contact with the gallbladder, and in 13% it was positioned between the abdominal wall and gallbladder. A safe percutaneous puncture was not possible in 34% of the patients (nine type IV gallbladders, 23 type I organs, and two type III gallbladders with anterior interposition of the colon).

Adult↗

PubMed2006

Ciliary neurotrophic factor restores gallbladder contractility in leptin-resistant obese diabetic mice.

BACKGROUND: Obesity and diabetes are major risk factors for cholesterol gallstones, and the majority of obese people are leptin-resistant. Our previous work has shown that both leptin-deficient (Lepob) and leptin-resistant (Lepdb) obese diabetic mice have decreased in vitro gallbladder motility. Leptin administration to leptin-deficient (Lepob) animals restores gallbladder motility and reverses obesity and hyperinsulinemia. However, additional leptin in leptin-resistant obesity would not be expected to improve obesity-related parameters. Recent studies demonstrate that ciliary neurotrophic factor (CNTF) reduces weight and hyperinsulinemia in leptin-resistant obesity. Our hypothesis is that CNFT would cause weight loss, lower blood sugars, and restore gallbladder contractility in leptin-resistant (Lepdb) mice. MATERIALS AND METHODS: 20 C57b/6J and 20 Lepdb 8-week-old female mice were injected daily with either intraperitoneal saline or 0.3 microg/g CNTFAx15 for 17 days. Gallbladders were mounted in muscle baths and stimulated with acetylcholine, neuropeptide Y, and cholecystokinin. Gallbladder volume, serum glucose, insulin, liver weight, liver fat, and gallbladder responses were measured. Data were analyzed by ANOVA. RESULTS: Saline treated obese mice had greater body weight and obesity parameters, but decreased gallbladder contractility to neurotransmitters compared to saline treated lean mice. CNTF administration to obese mice decreased body weight and obesity parameters, and restored gallbladder contractility. CNTF treated lean animals had weight loss and decreased gallbladder contraction to acetylcholine and cholecystokinin compared to saline treated lean animals. CONCLUSIONS: Ciliary neurotrophic factor (CNTF) causes 1) weight loss, 2) improvement of diabetes, and 3) alterations in gallbladder motility that is improved in obese mice but decreased in lean mice. We conclude that CNTF may improve gallbladder contractility in leptin-resistant obesity with diabetes.

Animals↗

PubMedDate not supplied

Gallbladder function before and after fundoplication.

No study has reported an association between gastroesophageal reflux disease (GERD) or its therapies and gallbladder function. We compared pre- and postoperative gallbladder function in patients undergoing fundoplication to determine the following: (1) whether patients with chronic GERD have preexisting gallbladder motor dysfunction; (2) whether medical or surgical therapy alters gallbladder function; and (3) whether division of the hepatic branch of the anterior vagus nerve is detrimental to gallbladder motility. Nineteen patients with documented GERD consented to a preoperative cholecystokinin-stimulated technetium hepatobiliary (CCK-HIDA) scan to quantify the gallbladder ejection fraction (GBEF). All patients underwent laparoscopic Nissen fundoplication. One month after fundoplication, 12 patients completed a repeat CCK-HIDA scan for determination of GBEF, with comparison to the preoperative GBEF. Among patients with preoperative GERD, 11 (58%) of 19 met the scintigraphic criteria for gallbladder dysfunction (GBEF <35%), which is a ratio comparable to that in patients undergoing a CCK-HIDA scan for presumed biliary dyskinesia during the same time period (31 [60%] of 53; P = NS, chi-square test) and exceeds the rate of abnormal GBEF reported in healthy volunteers (3%). Six of seven patients with a low preoperative GBEF who underwent repeat evaluation postoperatively had normalization of the GBEF (P < 0.05, paired t-test). In the 12 patients who underwent postoperative CCK-HIDA scanning, there was no association between preservation or division of the hepatic branch of the anterior vagus nerve and postoperative gallbladder dysfunction (P = NS, chi-square test). Unexpectedly, 58% of patients with GERD demonstrated gallbladder motor dysfunction prior to fundoplication, with improvement to normal occurring in most of those studied postoperatively. These data support controlled trials to determine the effect of chronic GERD and antisecretory therapy on gallbladder and global gastrointestinal smooth muscle function. Preservation of the hepatic branch of the anterior vagus nerve during fundoplication offered no clear benefit with regard to early postoperative gallbladder function.

Adult↗

PubMed2003

Gallbladder motility in obesity, diabetes mellitus and coeliac disease.

We reviewed data on gallbladder motility in obesity, diabetes and coeliac disease. In obesity, a condition characterised by increased risk of gallstone(s), decreased gallbladder motility has heterogeneously been reported as a consequence of the different type of meals used to induce gallbladder contraction, characteristics of the population studied, technique used, and proportion of patients with hyperinsulinaemia. Moreover, recent studies have evaluated the effect of dietary restriction on gallbladder motility in obese patients. A two- to three-fold increase in the risk of cholesterol gallstone(s) has been reported in diabetic patients, mainly in relation to obesity and hypertriglyceridaemia. Furthermore, decreased gallbladder motility has been described and attributed to other factors, including underlying autonomic neuropathy, reduced gallbladder sensitivity to cholecystokinin and/or reduced number of cholecystokinin receptors on the gallbladder wall. Impaired gallbladder motility has been reported also in patients with coeliac disease in relation to reduced secretion of enteric hormones and/or decreased gallbladder sensitivity to them. In particular, untreated coeliacs, when compared to controls, showed low postprandial cholecystokinin and increased fasting somatostatin levels. Interestingly, the correlation between fasting somatostatin levels and gallbladder size has clearly been confirmed in patients affected by somatostatinoma or treated with somatostatin or its analogues. Gallbladder motility can be affected by various clinical conditions, such as obesity, diabetes mellitus and coeliac disease.

Celiac Disease↗

PubMed2001

Cisapride improves gallbladder emptying in patients with type 2 diabetes mellitus.

BACKGROUND AND AIMS: Gallbladder motor function is impaired in many patients with diabetes, and may be related to cholinergic nerve damage. Cisapride is a prokinetic drug of the gastrointestinal tract and acts by releasing acetylcholine from cholinergic nerve endings. The aim of this study was to determine the effect of cisapride on gallbladder emptying in patients with type 2 diabetes mellitus (DM). METHODS: Gallbladder emptying and tests for autonomic neuropathy (AN) were performed in 27 patients with type 2 DM and in 10 healthy subjects. Gallbladder emptying was studied by using real-time ultrasonography after an overnight fast, and after the subjects received a breakfast that contained 2500 J. Gallbladder emptying was repeated after the treatment with cisapride (10 mg t.i.d.) for 1 week in all subjects. RESULTS: Abnormal gallbladder emptying was present in 14 (51.9%) patients. The residual gallbladder volume (mean +/- SEM) was higher (9.3 +/- 1.0 vs 4.6 +/- 0.6; P = 0.002), and ejection fraction was lower (57.4 +/- 4.0 vs 74.2 +/- 2.4; P = 0.015) in diabetic patients than it was in healthy subjects. Cisapride produced a reduction in fasting and residual volumes (24.6 +/- 2.4 vs 20.0 +/- 1.4; P = 0.034 and 9.3 +/- 1.0 vs 5.9 +/- 1.1; P = 0.00003, respectively), and an improvement in ejection fraction (57.4 +/- 4.0 vs 72.6 +/- 3.8; P = 0.000007). The improvement in gallbladder emptying after cisapride therapy was confined to the patients with AN (n = 13) (57.3 +/- 5.4 vs 80.4 +/- 2.9; P = 0.0017), suggesting denervation supersensitivity with an upregulation of cholinergic receptors. There was no significant change in the ejection fraction in patients without AN (57.5 +/- 6.1 vs 65.4 +/- 6.5; P = NS). Sex, duration of diabetes, peripheral neuropathy, diabetic retinopathy and serum cholesterol level did not influence gallbladder emptying. CONCLUSION: Impaired gallbladder emptying is common in patients with type 2 DM. Cisapride significantly improves gallbladder emptying in patients with autonomic neuropathy.

Acetylcholine↗

PubMed2004

The melatonin receptor subtype MT1 is expressed in human gallbladder epithelia.

Based on the fact that human bile and, particularly gallbladder bile, contains high physiological levels of the antioxidant melatonin, the aim of this study was to investigate whether the melatonin receptor MT1 is present in human gallbladder. Expression and localization of MT1 was assessed by RT-PCR, Western blotting and immunofluorescence analysis in gallbladder samples from patients with cholelithiasis and with advanced gallbladder carcinoma. Additionally, we monitored mRNA expression of the two key enzymes of melatonin synthesis, i.e. arylalkylamine-N-acetyltransferase (AANAT) and hydroxyindole-O-methyltransferase (HIOMT). MT1 mRNA and protein were present in all cholelithiasis (n = 10) and gallbladder carcinoma (n = 5) samples. As indicated from RT-PCR and Western blot studies, MT1 is located in gallbladder epithelia. Epithelial expression was further proven by immunofluorescence staining of MT1 in paraffin-embedded cholelithiasis and gallbladder carcinoma sections. Analysis of AANAT and HIOMT mRNA expression showed that HIOMT mRNA is present in gallbladder. Surprisingly, AANAT was not detectable under conditions where it was found in a human colon specimen. The absence of AANAT suggests that in human gallbladder, HIOMT might be involved in the formation of 5-hydroxytryptamine products other than melatonin. In summary, our results provide the first evidence for the presence of MT1 in human gallbladder epithelia. Therefore, in addition to its profound antioxidative effects in the biliary system, melatonin might also act through MT1-mediated signal transduction pathways. Thereby, it might be involved in the regulation of gallbladder function.

Acetylserotonin O-Methyltransferase↗

PubMed1999

Synthetic pathways of gallbladder mucosal prostanoids: the role of cyclooxygenase-1 and 2.

Acute cholecystitis is associated with increased gallbladder prostanoid formation and the inflammatory changes and prostanoid increases can be inhibited by nonsteroidal anti-inflammatory agents. Recent information indicates that prostanoids are produced by two cyclooxygenase (COX) enzymes, COX-1 and COX-2. The purpose of this study was to determine the COX enzymatic pathway in gallbladder mucosal cells involved in the production of prostanoids stimulated by inflammatory agents. Human gallbladder mucosal cells were isolated from cholecystectomy specimens and maintained in cell culture and studied in comparison with cells from a well differentiated gallbladder mucosal carcinoma cell line. COX enzymes were evaluated by Western immunoblotting and prostanoids were measured by ELISA. Unstimulated and stimulated cells were exposed to specific COX-1 and COX-2 inhibitors. In both normal and transformed cells constitutive COX-1 was evident and in gallbladder cancer cells lysophosphatidyl choline (LPC) induced the formation of constitutive COX-1 enzyme. While not detected in unstimulated normal mucosal cells and cancer cells, COX-2 protein was induced by both lipopolysaccharide (LPS) and LPC. Unstimulated gallbladder mucosal cells and cancer cells produced prostaglandin E2 (PGE2) and prostacyclin (6-keto prostaglandin F1alpha, 6-keto PGF1alpha) continuously. In freshly isolated normal gallbladder mucosal cells, continuously produced 6 keto PGF1alpha was inhibited by both COX-1 and COX-2 inhibitors while PGE2 levels were not affected. Both LPS and LPC stimulated PGE2 and 6 keto PGF1alpha formation were blocked by COX-2 inhibitors in freshly isolated, normal human gallbladder mucosal cells and in the gallbladder cancer cells. The prostanoid response of gallbladder cells stimulated by proinflammatory agents is inhibited by COX-2 inhibitors suggesting that these agents may be effective in treating the pain and inflammation of gallbladder disease.

6-Ketoprostaglandin F1 alpha↗

PubMed1991

[Sonographic study of gallbladder function: exogenous or endogenous stimulation?].

Eleven patients (8 male, 3 female, age 21-53 years) with dyspeptic symptoms and no gastrointestinal organic diseases were studied for their gallbladder contractile function. A comparative sonographic study of gallbladder contraction was performed after exogenous and endogenous stimulation. On day 1, ceruletide was infused at a dose of 2.5 ng/kg/min about 10 minutes. On day 2, a semi-liquid test meal of 1450 kJ (44 kJ% carbohydrates, 24 kJ% protein, 32 kJ% fat) was administered. Gallbladder volume was determined for 30 minutes before and 5, 10, 20, 30, 40, 60, 80, 100 and 120 minutes after both stimulations by means of realtime ultrasonography. Three diameters in two plains were measured for calculation of gallbladder volume. Following ceruletide, peak gallbladder contraction (range 7-48% of initial volume) was observed within 10 (n = 5) or 20 (n = 6) minutes. Following the test meal, peak gallbladder contraction ranged from 27-80% and was observed within 30 to 100 minutes. Variations in time and amount of peak gallbladder contraction does hardly allow to establish normal values. No significant correlation was found between both types of stimulation concerning peak gallbladder contraction or time to peak contraction. We conclude that for the assessment of gallbladder contractility, ceruletide infusion and determination of gallbladder volume after 20 minutes (upper range 48% of initial volume) is the most valuable procedure. Impaired gallbladder contractility can be diagnosed with certainty only after exogenous stimulation.

Adult↗

PubMed1991

Thermal ablation of the gallbladder.

Gallbladder ablation by means of injection of hot contrast medium was attempted in 13 dogs. Room temperature contrast medium was injected into the gallbladders of two additional dogs (controls). After midline laparotomy was performed to expose the gallbladder, temperature probes were placed in the liver adjacent to the gallbladder, and on the surface and in the lumen of the gallbladder. A 7-F catheter with multiple side holes was placed into the gallbladder. The cystic duct was clamped during the procedure. After injection of boiling contrast medium, the mean temperature in the gallbladder lumen was 80 degrees C; in the adjacent liver, 43.5 degrees C; and on the gallbladder surface, 45.8 degrees C. After the procedure, the cystic duct was unclamped, temperature probes and catheter were removed, and the laparotomy was closed in standard fashion. In the hot contrast medium group, one dog each was sacrificed at 2, 4, 8, and 12 weeks, and at 6 months. Six animals were sacrificed at 1 year. The gallbladder was completely ablated in 11 of 13 animals in the hot contrast medium group. One dog was sacrificed at 8 days because of bile leakage, and another was sacrificed at 17 days because of gallbladder rupture. The two control animals were sacrificed at 12 and 13 weeks, and their gallbladders were normal at that time.

Animals↗

PubMed1997

Reduced contractility and histological changes in the gallbladder due to portal hypertension in a hamster cirrhosis model.

BACKGROUND/AIMS: Little is known about the relationship of portal venous pressure to contractility and histological changes in the gallbladder. In this study, we investigated the relationship between portal hypertension and contractility and histological changes in the gallbladder in a hamster cirrhosis model. METHODS: Liver cirrhosis was induced in the hamsters (n = 20) by thioacetamide (TAA). Portal venous pressure was directly measured using a pressure-measuring instrument. The contractility of the gallbladder was appraised by the diameter before and after caerulein treatment. Gallbladder wall thickness and vessel areas in tissues were evaluated in relation to the portal venous pressure. RESULTS: The portal venous pressure, gallbladder wall thickness with submucosal edema and area of vessels in the gallbladder wall in the cirrhosis group were significantly increased compared with those in the control group (n = 20, receiving saline instead of TAA). The gallbladder contraction rate in the cirrhosis group was significantly decreased compared with that in the control group. In the cirrhosis group, there were positive correlations between the portal venous pressure and the gallbladder contraction rate, gallbladder wall thickness, and area of vessels. CONCLUSIONS: In the gallbladders of experimental cirrhotic hamsters, portal hypertension caused dilatation of the vessels as well as submucosal edema, and was an important factor in the increased thickness and reduced contractility of the gallbladder wall.

Animals↗

PubMedDate not supplied

Effect of intravenous fat on cholecystokinin secretion and gallbladder motility in man.

During total parenteral nutrition (TPN) gallbladder bile stasis and hypomotility have been well documented. Little is known, however, about the effect of the separate components of TPN on gallbladder motor function. Inasmuch as fat, administered intraduodenally, is a potent stimulus of cholecystokinin (CCK) secretion and gallbladder contraction we have investigated whether intravenous (IV) fat affects gallbladder motility. Six healthy volunteers were studied on two separate occasions, during infusion of Intralipid 10%, 200 mL/h or saline infusion (control) for 3 hours, to evaluate the effect of IV infusion of fat on (1) plasma CCK concentration and gallbladder volume and (2) CCK-induced gallbladder emptying. Intravenous infusion of Intralipid resulted in significant increases in serum triglycerides from 0.9 +/- 0.1 to 5.1 +/- 1.3 mmol/L (at 90 min). During fat infusion no significant changes in plasma CCK and gallbladder volume were noted when compared with basal values or to the control experiment. During IV fat, concomitant infusion of 0.25, 0.5, and 1.0 Ivy dog unit (IDU) per kilogram per hour of CCK-33 resulted in a significant reduction in gallbladder volume from 26 +/- 6 cm3 (basal) to 15 +/- 4 cm3 (p less than .05), 6 +/- 2 cm3 (p less than .05) and 2.5 +/- 1 cm3 (p less than .05), respectively. No significant differences in CCK-induced gallbladder emptying were observed between IV fat and saline infusion (control). It is concluded that, in contrast to intraduodenal fat, IV infusion of fat does not affect (1) basal plasma CCK and gallbladder volume and (2) CCK-induced gallbladder contraction.

Adult↗

PubMed2003

Arris & Gale lecture. Regulation and responses of gallbladder muscle activity in health and disease.

A complex relationship links biliary symptoms with the mechanisms of gallbladder emptying and the presence of gallstones. This relationship has been investigated by clinical studies of symptoms associated with gallstones, by investigation of gallbladder emptying and cholecystokinin (CCK) release in patients with gallstones, and after cholecystectomy, or truncal vagotomy, and in the irritable bowel syndrome (IBS). Laboratory studies examined receptor density on bovine gallbladder, and contractility of human gallbladder in response to a variety of stimuli was studied in vitro. A set of six symptoms associated with the presence of gallstones was identified; IBS appeared to be present in two-fifths of patients before cholecystectomy but only one-third of these patients had persistent IBS symptoms one year after operation. Gallbladder emptying studies confirmed the poor contraction of stone-bearing gallbladders; abnormal patterns of emptying were also found in patients with IBS. Gallbladder emptying and filling appear to be largely neurally regulated. CCK receptor density was very low in gallbladder tissue, suggesting that receptors on nerve cells might mediate the action of CCK. Relaxation of gallbladder muscle was mediated by adrenergic and nitrergic nerves. The inflammatory mediator bradykinin, however, had a strong direct action on muscle cells to cause gallbladder contraction. The work reported here gives an overview of the symptoms and mechanisms of disease associated with the presence of stones in the gallbladder.

Cholelithiasis↗