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PubMed1996

Acute effect of ursodeoxycholic acid on gallbladder volume in healthy subjects.

BACKGROUND: Although it has been shown that chronic administration of ursodeoxycholic acid increases gallbladder fasting and residual volume, it is unknown whether ursodeoxycholic acid exerts an acute effect on gallbladder volume. We therefore evaluated the effect of a single oral dose of ursodeoxycholic acid on gallbladder volume in healthy volunteers. METHODS: After the volunteers had fasted overnight, gallbladder volume was measured sonographically every 15 min for 5 h. Following a 1-h control period group I (n = 8) received ursodeoxycholic acid (1000 mg) orally with 100 ml of water, whereas group II (n = 8) received 100 ml of water (placebo) only. Gallbladder volumes were calculated, applying the sum-of-cylinders method. Serum levels of ursodeoxycholic acid were determined by gas chromatography at 1-h intervals. RESULTS: Gallbladder fasting volumes before ursodeoxycholic acid were similar in both groups (24.0 +/- 2.3 ml versus 25.4 +/- 3.3 ml; NS). After ingestion of ursodeoxycholic acid (group I) gallbladder volume increased rapidly, reaching 27.6 +/- 3.1 ml (p < 0.04) 1 h and 38.4 +/- 3.4 ml (p < 0.02) 4 h after ingestion of ursodeoxycholic acid. The individual gallbladder volumes after ingestion of ursodeoxycholic acid in group I increased to 146%-211% of pretreatment values. Ursodeoxycholic acid serum levels increased from 0.94 +/- 0.38 mumol/l to 10.51 +/- 1.36 mumol/l (p < 0.001) and correlated closely with gallbladder volumes (r = 0.80; p < 0.05). After ingestion of water only (group II) gallbladder volume decreased transiently from 15 min to 30 min after water intake and then remained at pretreatment values throughout the study period. CONCLUSION: Administration of a single oral dose of ursodeoxycholic acid causes a rapid increase in gallbladder volume, which reaches 163 +/- 10% of pretreatment volume at 4 h and is closely correlated with ursodeoxycholic acid serum levels.

Adult↗

PubMed1997

Gallbladder motility change in late pregnancy and after delivery.

OBJECTIVES: The incidence of gallstone disease has increased recently in Korea and there seems to be an increased prevalence of gallstones when in association with pregnancy. Although the pathogenesis is incompletely defined, and altered motility of the gallbladder may contribute to the increased risk of gallstones during pregnancy. METHODS: We measured gallbladder volume using real-time ultrasonography to find out the mechanism for the changes of gallbladder motility during late pregnancy. Eighteen pregnant women took the gallbladder ultrasonography during their last trimester of pregnancy and after delivery; gallbladder volume and ejection fraction were calculated in each patient. RESULTS: Fasting gallbladder volumes increased significantly in the last trimester of pregnancy (25.28 +/- 14.26ml) compared with postpartum (17.44 +/- 5.82 ml) (p < 0.05). Gallbladder volumes measured after fatty meals showed more increment in pregnant women (10.13 +/- 7.19 ml) than in those after delivery (4.34 +/- 3.36 ml) (p < 0.005). A significantly reduced gallbladder ejection fraction was found in the pregnant group (60.56 +/- 18.80%) compared with those after delivery (77.48 +/- 13.37%) (p < 0.005). CONCLUSION: Gallbladder motility in late pregnancy shows significant impairment compared with that in postpartum. Thus, we suggest that gallbladder hypomotility may occur during late pregnancy, and this impairment of gallbladder motility may play an important role in gallstone formation.

Adult↗

PubMed2006

[Clinicopathologic features of gallbladder adenocarcinoma with marked stromal fibrosis--a report of 19 cases].

BACKGROUND & OBJECTIVE: Macropathologic types of gallbladder cancer are mostly polyp type, intumescent type, and cauliflower form lump. Its histological types include well or poorly differentiated adenocarcinoma, mucinous adenocarcinoma, and undifferentiated cancer. This research was to explore the clinicopathologic features of gallbladder adenocarcinoma with marked stromal fibrosis. METHODS: Pathology of 19 cases of gallbladder adenocarcinoma with marked stromal fibrosis was observed using a light microscopy and SP immunohistochemistry. Clinicopathologic features of 19 patients were analyzed. RESULTS: Most of the patients had long-term history of cholecystitis gallbladder calculus. B ultrasound showed that the gallbladder wall was irregularly thickened or presented nodosity. Observed with naked eyes, gallbladder adenocarcinoma with marked stromal fibrosis did not form cancer nodule and extrude into the gallbladder lumen, the gallbladder wall showed regional thickening, a few cases showed diffuse irregular thickening. Observed under a light microscope, the adenocarcinoma cells were mostly arranged as single layers, seldom arranged as multiple layers, and formed adenoid structures with different sizes, various shapes, and irregular arrangement; the nuclei were heterogenic with haryomitosis presented in a few cases; inflammatory cells were infiltrated in hyperplastic fibrous connective tissue of some cases. According to immune phenotyping, CK (AE1/AE3), CK (AE1), CK7 (OV-TL12/30), CK8 (C51), CK18 (Dc-10), CK19 (RCK108), and EMA (Mc-5) showed strong expression, CEA (COL-1), CK20 (Ks20. 4), and MUC-5AC (CLH2) showed moderate expression, and MUC-2 (B306. 1) showed weak expression; CK17 (E3) showed focal expression. CONCLUSIONS: The clinical manifestation, macropathologic type, histological characteristics of gallbladder adenocarcinoma with stromal fibrosis are different from other types of adenocarcinoma. Its genesis may be related to chronic cholecystitis: long-term inflammation causes regional hyperplasia and heterogeneity of the gland body, lead to focal or regional thickening of the gallbladder wall, and result in gallbladder adenocarcinoma with stromal fibrosis finally.

Adenocarcinoma↗

PubMed1995

Effect of erythromycin on gallbladder emptying in patients with antrectomy or truncal vagotomy.

OBJECTIVES: Erythromycin, a motilin-like agent, stimulates gallbladder contraction in healthy control subjects. Because the action of erythromycin is cholinergic dependent and possibly related to premature phase III migrating motor complex activity in the antrum, we investigated the effect of erythromycin on gallbladder volume in six patients with truncal vagotomy without gastric resection and 14 patients with antrectomy (6 with Billroth I anastomosis, 8 with Billroth II anastomosis), and we compared the results obtained with those in eight healthy controls. In addition, the effect of meal ingestion on gallbladder volume was studied. METHODS: Gallbladder volumes, measured with ultrasonography, were determined every 15 min for 180 min after erythromycin infusion (3 mg/kg i.v.), as well as 30 and 60 min after meal ingestion. RESULTS: Basal gallbladder volumes were not significantly different among the four groups. Erythromycin induced a significant (p < 0.01-0.05) gallbladder contraction of maximal 46 +/- 6% in the controls, 49 +/- 9% in the patients with truncal vagotomy, and 38 +/- 7% in the patients with antrectomy and Billroth I anastomosis. In the patients with antrectomy and Billroth II anastomosis, no significant reduction in gallbladder volume after erythromycin was observed. Meal-induced gallbladder contraction was normal in all patients, including those with Billroth II anastomosis. CONCLUSIONS: These results indicate that neither the long vagus nerve nor the antrum is essential for erythromycin-induced effects on the gallbladder. Because no significant reduction in gallbladder volume in response to erythromycin was observed in the patients with antrectomy and Billroth II anastomosis, we suggest that duodenojejunal anatomical integrity is essential for erythromycin-induced gallbladder contraction.

Adult↗

PubMed1996

Gallbladder contraction capacity in response to liquid fatty meal: a real time ultrasonographic study.

Gallbladder contraction in response to a liquid fatty meal was studied in a hundred consecutive adult Thai subjects by using an ultrasound machine. None of them had clinical evidence of hepato-biliary and gastric diseases. The gallbladder sizes were detected at the fasting stage and after taking a liquid fatty meal (250 ml of milk) at 30, 60, 90 and 120 minutes respectively. The gallbladder size was measured by two methods, the surface area (SA) along its longitudinal plane and gallbladder volume (VOL). The percentage of maximal reduction of gallbladder size in each individual was considered as the gallbladder contraction capacity. The average contraction capacity in this group was 57.88% +/- 12.38% by SA or 74.47% +/- 9.96% by VOL. The variation of gallbladder contraction capacity in this population was found to have a normal curve distribution. The maximal contractions were found mostly (69%) at 60 minutes and 93% of subjects had maximal contractions within 90 minutes. There was no difference in gallbladder contraction capacity between males and females and also among different age groups. The tenth percentile of gallbladder contraction capacity was 41.12% by SA or 61.82% by VOL. We propose that these should be considered as the lower limit of normal gallbladder contraction capacity after taking 250 ml of liquid fatty meal. This test was simple, safe and easily measured. This may provide useful basic information for further functional study of gallbladder diseases.

Adult↗

PubMedDate not supplied

Action of cisapride on gallbladder contraction in patients with diabetes mellitus.

BACKGROUND/AIMS: Gallbladder emptying abnormalities are common in patients with diabetes mellitus, and it has been hypothesized that they contribute to the increased incidence of gallbladder stones and biliary pain observed in these patients. Cisapride is a drug that exerts a prokinetic effect in both animals and humans. Recently, we demonstrated that cisapride decreased the fasting and post-prandial gallbladder volume in healthy subjects. Therefore, we investigated the action of cisapride on gallbladder contraction in diabetic patients. METHODOLOGY: Twenty diabetes mellitus patients and 20 healthy volunteers participated in this study. On the day of the study, ultrasonography was performed at 9 am, after 12 hours of fasting. After the basal measurement was obtained, the diabetic patients and healthy subjects received 10 mg cisapride or a placebo peroral. Two hours later, gallbladder volumes were rescanned by ultrasonography at 15-minute intervals for 60 minutes. RESULTS: The fasting gallbladder volume was 19.8 +/- 6.7 ml in the diabetic patients, and after the administration of cisapride, the gallbladder volume decreased by 32.2%-38.6% as compared to the baseline (p<0.02, 0.05, 0.01) and by 35.0%-45.8% as compared to the diabetic controls (p<0.02, 0.05, 0.001). In the healthy subjects, cisapride did not change the fasting mean gallbladder volume as compared to the baseline. After the administration of cisapride in the diabetic patients, the mean gallbladder volume decreased more than in the healthy subjects. The mean gallbladder volumes of the diabetic patients were between 12.1 +/- 4.2-13.4 +/- 4.2 ml. In the healthy volunteers, after the administration of cisapride, the volume was reduced by 1.9%-11.3% as compared to the healthy control group, but the volume changes of these two groups were not statistically significant. CONCLUSION: This study shows that the administration of cisapride causes gallbladder volume reduction in diabetic patients.

Cisapride↗

PubMed1989

Evaluation of prostacyclin production by human gallbladder.

The prostanoids have been demonstrated to be involved in gallbladder physiology and disease. In previous reports, prostaglandin E (PGE) compounds were found to be increased in inflamed human gallbladders. Prostaglandin synthetase inhibition decreased PGE formation by human gallbladders; however, the relief of symptoms of cholecystitis did not correlate well with the decrease in PGE formation. This suggested that other prostanoids may be involved in cholecystitis. The purpose of this study was to evaluate the production of the proinflammatory arachidonic acid metabolite prostacyclin by gallbladders from patients with calculous cholecystitis. The formation of PGE and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), the stable metabolite of prostacyclin, in normal human gallbladder mucosal cells and muscle tissue was compared with that produced by diseased mucosal cells and muscle tissue. Normal human gallbladders produced small amounts of 6-keto-PGF1 alpha, and no differences in formation rates were evident when muscle tissue was compared with mucosal cells. Diseased gallbladders produced significantly greater amounts of 6-keto-PGF1 alpha than did normal gallbladders, and diseased gallbladder muscle produced approximately four times greater amounts of 6-keto-PGF1 alpha than did diseased gallbladder mucosa. Prostacyclin formation is increased in diseased human gallbladders and may be an important mediator of the inflammatory changes of cholecystitis.

Acute Disease↗

PubMed2005

Copper, zinc, and Cu/Zn ratio in carcinoma of the gallbladder.

INTRODUCTION: The exact role of copper and zinc in the etiology of carcinoma of the gallbladder is unclear. Some studies suggest the Cu/Zn ratio is a good indicator of the extent and prognosis in carcinoma of the gastrointestinal tract. The aim of the present study is to estimate the micronutrient profile and Cu/Zn ratio in the serum, tissues, and bile of patients with benign and malignant gallbladder diseases. METHODS: The present study was carried out in 60 patients comprising 30 each of carcinoma of the gallbladder and cholelithiasis, and 30 age and sex matched controls. Copper and zinc levels were estimated in blood, bile, and tissue using a Perkin Elmer Model 2380 Atomic absorption Spectrophotometer. RESULTS: The mean serum zinc levels were significantly lower in patients with carcinoma of the gallbladder than in patients with cholelithiasis and in healthy controls (P < 0.001). The mean serum copper levels were significantly higher in patients with carcinoma of the gallbladder as compared to patients with cholelithiasis and healthy controls (P < 0.001). Biliary and tissue zinc levels were significantly lower in patients with carcinoma of the gallbladder than in patients with cholelithiasis. Biliary and tissue copper levels were higher in patients with carcinoma of the gallbladder than in patients with cholelithiasis. The serum Cu/Zn ratio showed a gradual and significant increase from 1.11 in healthy controls to 1.35 in patients with cholelithiasis and 2.12 in patients with carcinoma of the gallbladder. The biliary and tissue Cu/Zn ratios were also significantly increased in patients with carcinoma of the gallbladder than in patients with cholelithiasis (P < 0.001). CONCLUSIONS: Our data support an association between lower zinc levels and consequently an increased Cu/Zn ratio and carcinoma of the gallbladder. Whether zinc supplementation has a protective effect in preventing carcinoma of the gallbladder needs to be studied further.

Bile↗

PubMed1999

Altered gallbladder bile acidification with long-term total parenteral nutrition.

BACKGROUND: An important function of the gallbladder is to acidify and concentrate bile. Acidification helps protect against the precipitation of calcium salts, which promote gallstone formation. Altered acidification may result in pigment gallstones. We investigated gallbladder composition in a model of TPN-associated pigment gallstones to test whether changes in acidification may be important in this gallstone model. MATERIALS AND METHODS: Ten miniswine were intravenously fed for 21 to 27 days (mean 23 days). Ten fed pig chow with intravenous infusion of saline served as controls. Gallbladder and hepatic bile electrolytes, lipids, pH, and pCO2 were measured. RESULTS: All animals remained healthy and gained weight. Hepatic bile electrolytes and pH were similar among all animals. Pigs on TPN had a higher gallbladder pH and the [H+] was half the value of controls [8.1 +/- 1.6 x 10(-8) meq/liter (control) versus 3.9 +/- 0.7 x 10(-8) meq/liter (TPN)]. Gallbladder bile pCO2, sodium (Na), and potassium were higher in controls. Biliary lipids [bile salts (BS), phospholipids, and cholesterol] with TPN were decreased in both hepatic and gallbladder bile. CONCLUSIONS: Unlike short-term TPN where gallbladder pH and [BS] are similar, with long-term TPN pH is higher with lower [H+], [Na], and [BS]. Despite a presumed longer residence time in the gallbladder, intravenous feeding without oral intake results in gallbladder bile that is less concentrated and acidified. Enteral stimulation may be an important stimulus for gallbladder acidification and periods without feeding may promote gallstone formation by increasing the pH of gallbladder bile.

Animals↗

PubMed1989

Effect of bradykinin on feline gallbladder water transport and prostanoid formation.

Continuing evaluation of the pathophysiology of gallbladder disease has demonstrated significant relationships between gallbladder mucosal fluid transport, gallbladder inflammation, and prostanoid formation. Inflamed gallbladder mucosa secretes, rather than absorbs, fluid, a process associated with prostaglandin formation. Bradykinin has been previously implicated in the pathogenesis of cholecystitis and, in the intestine, bradykinin stimulates mucosal fluid secretion by a prostaglandin-mediated mechanism. Bradykinin was infused into the gallbladder lumen and administered intraarterially into the hepatic artery of perfused cat gallbladders. Both methods of bradykinin administration reversed the mucosal absorption present during control experiments as measured by concentration changes in a nonabsorbable marker. Perfusate and gallbladder tissue prostaglandin E concentrations were significantly increased by bradykinin when compared to control values. Concentrations of 6-keto PGF1 alpha in perfusate solutions and in gallbladder tissue were significantly increased, suggesting bradykinin increased prostacyclin formation. Bradykinin administration significantly increased inflammation, as evaluated by a histologic scoring system. Indomethacin was administered intravenously along with luminal perfusion of the gallbladder with bradykinin. Indomethacin significantly decreased gallbladder fluid secretion and prostanoid formation, but not histologic inflammation, when compared to values produced by bradykinin alone. An increase in systemic vascular and bile kinin concentrations produces gallbladder mucosal water secretion, a process which may be mediated by prostanoids. Histologic inflammation produced by bradykinin was not prevented by indomethacin.

6-Ketoprostaglandin F1 alpha↗

PubMedDate not supplied

Radical operations for carcinoma of the gallbladder: present status in Germany.

Despite the overall poor prognosis of gallbladder carcinoma, it appears that, in resectable lesions, an aggressive surgical approach promises improvement in survival rates. Radical treatment of gallbladder carcinoma is based on a detailed knowledge of the lymphatic, venous, direct, and intraductal modes of spread of gallbladder carcinoma. Customized therapy of gallbladder carcinoma takes staging into consideration: if one is dealing with gallbladder carcinoma with macroscopic liver infiltration (T3 or T4), or with a pre- or intraoperatively diagnosed gallbladder carcinoma with an unknown depth of infiltration, an en bloc resection of the gallbladder with adjacent liver segments IVb and V, perhaps including IV, as well as a dissection of the hepatoduodenal ligament should be performed. If the carcinoma is missed intraoperatively at the time of cholecystectomy for other indications, in the presence of a T2 gallbladder carcinoma in proximity to the liver bed, reoperation with dissection of the hepatoduodenal ligament and resection of liver segments IVb and V should be performed. In the presence of T1 gallbladder carcinoma, simple cholecystectomy is adequate. This concept is based on our experience with 113 patients with gallbladder carcinoma who underwent treatment in our department from January, 1970 to June, 1989. Sixty-seven percent of the gallbladder carcinomas were resected, 30% for cure and 37% palliatively. In 33%, the operation was limited to an exploratory laparotomy or a palliative operation, or no operation was performed. Of the curatively resected carcinomas (n = 34), 7 were Stage I, 7 Stage II, 9 Stage III, and 11 Stage IV.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗

PubMedDate not supplied

Percutaneous transcholecystic biliary interventions using gallbladder anchors: feasibility study in the swine.

The purpose of this study was to report our initial experience with a swine model for biliary interventions by using a percutaneous transcholecystic access after suture anchor of the gallbladder. Telepaque tablets were given to five pigs to opacify the gallbladder. Under fluoroscopy, the opacified gallbladder was punctured percutaneously and three suture anchors were used to fix the anterior wall of the gallbladder to the abdominal wall. Two weeks later, the gallbladder was punctured and access into the distal common bile was obtained through the cystic duct. Balloon expandable stents were deployed into the distal common bile duct. Follow-up cholangiograms were obtained at 1 and 2 weeks. Necropsy was performed after 2 weeks to evaluate the relationship between the gallbladder and abdominal wall. Suture anchor placement was successful in all five pigs. One pig with a deep and highly positioned gallbladder developed fever, anorexia, and vomiting secondary to excessive stretch of the gallbladder. Placement of the guidewire through the extremely tortuous and small cystic ducts proved to be the most challenging step of the procedure. Metallic stents were successfully deployed in all four pigs in which it was attempted. Four animals tolerated the procedures without changes in their clinical conditions and no symptoms. Successful follow-up cholangiograms were performed at 1 and 2 weeks post-stent deployment without complications. All stents remained patent during the follow-up period. Necropsy demonstrated close attachment and adherence of the gallbladders to the antero-lateral abdominal wall in all four animals. Suture anchoring of the gallbladder is feasible in most pigs with superficially located gallbladders. This technique allows a safe and repeat access into the biliary system using a transcholecystic approach.

Animals↗

PubMed2000

The fetal gallbladder: morphology and morphometry by microdissection.

Most studies of the fetal gallbladder have been performed using ultrasonography. The identification of the fetal gallbladder and the presence of gallstones have been determined this way. The purpose of this study was to investigate the morphology and morphometry of the actual fetal gallbladder by microdissection and to examine its internal features and content. Eighty-nine formalin-embalmed fetuses of CR age 35 mm to 342 mm, i.e. 10 weeks to 36 weeks gestational age (GA), were studied by hepatic evisceration. The fetal gallbladder was examined in-situ in its bed, in relation to the umbilical vein, the anterior hepatic margin and its protrusion below the inferior hepatic surface of the liver. After excision, the form, length and diameters of the gallbladder were determined and its internal surface, lumen and content also examined. The mean length of the fetal gallbladder for the gestational ages studied ranged from 2.21 mm (10 weeks GA) to 281.6 mm (32 weeks GA); the mean fundal diameter ranged from 0.4 mm (one specimen only) to 9.42.4 mm for the same period, while the infundibular width ranged from 0.41 mm (one specimen only) to 9.01.6 mm, and the antero-posterior diameter at the fundus ranged from 0.90.3 mm to 9.03.3 mm for the same period. The parameters of the gallbladder for the period examined showed a curvilinear increase in size and were consistent with the ultrasonographic studies. The distance of the fetal gallbladder from the umbilical vein was variable and, as the gallbladder lengthened, the fundus encroached the anterior hepatic margin towards 34 weeks. A descent of the gallbladder from an "intra-hepatic" position early in fetal life to a sub-hepatic position later was clearly evident. The gallbladder wall was thick in early fetal life (10-13 weeks GA) and contained crumbly debris. Bile staining occurred at 14 weeks gestational age and the mucosa took on the normal appearance with the bile having an adult colour and consistency at 20 weeks GA.

Dissection↗

PubMed1987

Pancreatic polypeptide enhances postcontractile gallbladder filling in the prairie dog.

The hypothesis that pancreatic polypeptide promotes postcontractile gallbladder filling was tested in the prairie dog model. Fifteen animals underwent laparotomy with catheter placement into the gallbladder, distal common bile duct (vent), and femoral vein. The gallbladder was perfused with [14C]polyethylene glycol labeled lactated Ringer's solution at 0.03 ml/min and vent effluent was collected at 2.5-min intervals. All animals received a 20-min intravenous infusion of cholecystokinin-octapeptide, 2.5 ng/kg X min, immediately followed by 60-min infusions of either lactated Ringer's solution or bovine pancreatic polypeptide (PP), 10 or 50 ng/kg X min. Gallbladder emptying and intragallbladder pressure were similar for all three groups after cholecystokinin-octapeptide. When lactated Ringer's was administered after cholecystokinin-octapeptide, gallbladder filling increased by 15.6% with a minimal change in gallbladder pressure. In contrast, infusion of PP10 resulted in a significant (p less than 0.02) increase in gallbladder filling, 64.1% +/- 17.1%, and a significant (p less than 0.05) decrease in intragallbladder pressure, as compared to controls. Similar findings were noted with PP50. These data indicate that exogenous PP significantly increases gallbladder filling after cholecystokinin-induced gallbladder contraction. This enhanced filling results from gallbladder relaxation as manifested by decreased intraluminal pressure. These findings coupled with the observation that serum PP levels remain elevated for up to 6 h after a meal suggest that PP may play a role in the regulation of postprandial gallbladder filling.

Animals↗

PubMed1990

Effects of ursodeoxycholic acid on gallbladder contraction and cholecystokinin release in gallstone patients and normal subjects.

It has been previously suggested that treatment with ursodeoxycholic acid leads to decreased gallbladder emptying. The proposed mechanism is decreased release of cholecystokinin through negative feedback control by an increased amount of intraduodenal bile acids. In the present study we examined cholecystokinin release and gallbladder contraction after oral administration of a commercial fatty meal (Sorbitract; Dagra, Diemen, The Netherlands) using ultrasonography in eight normal subjects and eight gallstone patients before and after 1 and 4 weeks of treatment with ursodeoxycholic acid (10 mg kg-1.day-1). Fasting gallbladder volume increased in 15 of 16 subjects during treatment (P less than 0.01). Minimal volume did not change. Therefore, both absolute and relative gallbladder emptying increased during therapy. Maximal decrement of gallbladder volume in milliliters and percentage as well as integrated gallbladder contraction during 90 minutes in milliliters and percentage were significantly increased after 1 and 4 weeks of treatment with ursodeoxycholic acid when compared with data before therapy. Gallstone patients tended to have larger fasting and residual gallbladder volumes than normal subjects, whereas parameters for the amount of bile expelled (maximal decrement of gallbladder volume and integrated gallbladder contraction in milliliters and percentage) did not differ. Release of cholecystokinin did not change during treatment and did not differ significantly between patients and normal subjects. Mean relative percentage of ursodeoxycholic acid in bile during treatment in 13 subjects consenting to have duodenal intubation was 47% (range 31%-60%). Changes of fasting gallbladder volume after institution of bile acid treatment correlated significantly (r = 0.74, P less than 0.01) with changes of cholesterol saturation index but not with relative percentage of ursodeoxycholic acid in bile. This study indicates that gallbladder emptying does not decrease during treatment with ursodeoxycholic acid. Moreover, there is no evidence of decreased cholecystokinin release.

Adult↗

PubMed1992

Antral control of gallbladder cyclic motor activity in the fasting state.

The hypothesis that gastric antrum controls the phasic contractions of gallbladder cyclic motor activity in the fasting state was tested. Gallbladder, gastric, and small bowel motor and myoelectric activity was recorded by strain gauge transducers and bipolar electrodes. Gallbladder pressure was measured manometrically by a surgically implanted intraluminal catheter. After control recordings for 4 to 6 weeks, antrectomy and gastroduodenostomy were performed. Six weeks later, bilateral truncal vagotomy was performed in each dog. Recordings were made after each surgical procedure. In the control state, the gallbladder exhibited cyclic motor activity consisting of phasic contractions at a frequency of 0.75 +/- 0.02/min superimposed on an increase in baseline pressure. Antrectomy and gastroduodenostomy completely abolished the phasic contractions of gallbladder cyclic motor activity and significantly decreased the incidence of the cyclic increase in baseline pressure. Subsequent vagotomy had no additional effect on gallbladder cyclic motor activity. In intact dogs, the gallbladder filled from 0% to 80% and emptied from 80% to 100% of the duodenal migrating motor complex cycle, which was considered to begin at the start of phase I activity. Antrectomy significantly altered this pattern; after antrectomy, the gallbladder filled from 0% to 10% and from 90% to 100% and emptied during the remainder of the duodenal migrating motor complex cycle. Subsequent vagotomy had no additional effect on periodic gallbladder filling and emptying. It is concluded that major changes occur in gallbladder cyclic motor activity and its periodic filling and emptying pattern in the fasting state after antrectomy and vagotomy. It is hypothesized that in the absence of cyclic phasic contractions after antrectomy, periodic stirring and agitation of gallbladder bile and its mixing with fresh hepatic bile may not occur in the fasting state. The absence of this phenomenon may lead to supersaturation of bile near the mucosal surface and increase the propensity for precipitation of salts and formation of gallstones.

Animals↗

PubMed1995

Taurodeoxycholic acid stimulates rabbit gallbladder eicosanoid release.

Rabbit common bile duct ligation has been shown to concomitantly increase levels of gallbladder taurodeoxycholic acid and gallbladder eicosanoid release. This study examines the hypothesis that taurodeoxycholic acid, a known chemical mediator of gallbladder inflammation, stimulates endogenous gallbladder eicosanoid release. Male New Zealand white rabbits were anesthetized, gallbladders removed and perfused in vitro with Krebs-Henseleit buffer (pH 7.4, 37 degrees C) at 1 ml/min with increasing doses of taurodeoxycholic acid (0, 10, 30 and 100 mM) added to the perfusate. The effluent was collected at 15, 30, 60 and 120 min of perfusion and assayed for 6-keto-PGF1 alpha (PGI2 metabolite), PGE2, and thromboxane B2 (TXB2) by enzyme immunoassay. Taurodeoxycholic acid increased gallbladder eicosanoid release in a dose-related manner with 6-keto-PGF1 alpha and PGE2 release 10-fold higher than TXB2. Indomethacin (1.5 mM) decreased gallbladder eicosanoid release by 50% in the gallbladders perfused with 30 mM taurodeoxycholic acid, demonstrating that the increased gallbladder eicosanoid release was due to de novo synthesis. These findings suggest that the increased release of gallbladder PGI2 and PGE2 described in animal models of cholecystitis may, in part, be related to increased gallbladder bile levels of taurodeoxycholic acid.

6-Ketoprostaglandin F1 alpha↗

PubMed2000

Preoperative evaluation to predict technical difficulties of laparoscopic cholecystectomy on the basis of histological inflammation findings on resected gallbladder.

BACKGROUND: No papers have heretofore documented histological studies of cases involving the inflammation of resected gallbladder or examined surgical difficulties on the basis of pathological findings. METHODS: On the basis of the histological inflammation findings on the resected gallbladders of 437 patients who underwent laparoscopic cholecystectomy (LC), the factors affecting the technical difficulty of the operation were examined through preoperative clinical findings (13 items), diagnostic imaging (22 items), and blood test findings (6 items), using multivariate analysis. RESULTS: In accordance with the four-stage classification of inflammation findings for the resected gallbladder, the inflammation findings on the resected gallbladder indicated a higher correlation with the time required for gallbladder dissection (30.2 +/- 16.3 minutes) than with the operation time (77.6 +/- 32.7 minutes). Thus, the technical difficulty of the operation was judged according to the time required for gallbladder dissection. For the preoperative findings on 418 patients who underwent successful LC, the most influential factors on the time required for gallbladder dissection were the presence of abnormal findings on computed tomography, the degree of fever, obesity index, nonvisualized gallbladder cholangiography, and cystic duct length. According to the multiple regression equation of these five factors, the gallbladder dissection for the 19 patients who underwent conversion to open cholecystectomy (OC) due to extreme inflammation was calculated to require 61.9 +/- 12.3 minutes, and the patients who showed a gallbladder dissection time longer than 49.6 minutes were judged to have high technical difficulty predicted from the preoperative evaluation. In the preoperative evaluation, sensitivity was 79.6%, specificity was 97.6%, accuracy was 95.0%, positive predictive value was 85.0%, and negative predictive value was 96.6%. Next, each finding was scored on the basis of a multiple regression equation of five factors, and the technical difficulty of the operation was quantified using these scores. The score of the patients who underwent conversion to OC was 8.0 +/- 2.0, and the patients who showed a score higher than 6 were judged to have high technical difficulty. Almost the same results as in the aforementioned preoperative evaluation were obtained using these scores. CONCLUSION: The judgment using the scores was satisfactory in terms of the simplicity of evaluating the technical difficulties associated with each patient and the ease of obtaining information for each factor. The quantification of technical difficulty using the scores is useful for preoperative prediction of which patients will have difficulties in gallbladder dissection and the conversion to OC in LC. Our results suggest that the consideration of technical difficulties is important for conducting safe operations with avoiding intraoperative complications.

Adult↗