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Background: Intraduodenal bile salts exert negative feedback control on postprandial gall bladder emptying., Aims: We wished to examine whether a similar control mechanism occurs in the fasting state., Methods: Intraduodenal bile salt depletion was achieved by 12 g of cholestyramine. Thereafter, in study A (seven subjects), the effects on gall bladder volume (by ultrasound) and antroduodenal motility of intraduodenal infusions of taurocholate egg yolk-phosphatidylcholine micelles were assessed. In study B (nine subjects), the effects on gall bladder volume of infusing mixed micelles composed of taurocholate (100 mM) and low (26 mM) or high (68 mM) amounts of egg yolk-phosphatidylcholine, or low amounts of dipalmitoylphosphatidylcholine were determined., Results: Cholestyramine induced strong and prolonged gall bladder contraction without cholecystokinin release. In study A, micellar infusions increased gall bladder volume without affecting migrating motor complex cycle length. In study B, intraduodenal infusion induced strong increases in gall bladder volume in the case of taurocholate micelles containing low amounts of egg yolk-phosphatidylcholine, moderate increases in micelles containing low amounts of dipalmitoylphosphatidylcholine but no change in micelles containing high amounts of egg yolk-phosphatidylcholine, in all cases without altered plasma cholecystokinin levels. Phosphatidylcholine hydrolysis was significantly higher after infusion of egg yolk-phosphatidylcholine compared with infusion of dipalmitoylphosphatidylcholine containing micelles. Intermixed micellar-vesicular bile salt concentrations (responsible for detergent effects) were higher in egg yolk-phosphatidylcholine than in dipalmitoylphosphatidylcholine containing model biles and if lyso-phosphatidylcholine was included., Conclusions: Intraduodenal bile salts exert negative feedback on fasting gall bladder volume. The modulating effects of various phospholipids may relate to their effects on intermixed micellar-vesicular bile salt concentrations.

Background: It has been suggested that slow transit constipation (STC) may be part of a panenteric motor disorder., Aim: To evaluate motility of an upper gastrointestinal organ, the gall bladder, in 16 patients with STC and 20 healthy controls., Methods: Gall bladder emptying (ultrasonography) was studied in response to neural, cephalic-vagal stimulation with modified sham feeding (MSF) for 90 minutes and in response to hormonal stimulation with cholecystokinin (CCK, 0.5 IDU/kg/h) for 60 minutes., Results: Fasting gall bladder volume in patients with STC (17 (2) cm(3)) was significantly (p<0. 01) reduced compared with that in controls (24 (2) cm(3)). Gall bladder emptying in response to MSF was significantly reduced in patients with STC expressed both as percentage emptying (11 (5)% versus 22 (3)%; p<0.05) and as absolute emptying (2.1 (0.7) cm(3) versus 4.9 (0.7) cm(3); p<0.02). However, percentage gall bladder emptying in response to CCK was not different between patients and controls (73 (4)% versus 67 (4)%) although the absolute reduction in gall bladder volume was significantly (p<0.05) smaller in patients (10.7 (1.1) cm(3) versus 15.3 (1.4) cm(3))., Conclusions: Patients with slow transit constipation have smaller fasting gall bladder volumes, impaired gall bladder responses to vagal cholinergic stimulation, but normal gall bladder responses to hormonal stimulation with CCK. These results point to abnormalities in gastrointestinal motility proximal from the colon in slow transit constipation and more specifically, impaired neural responsiveness.

Current evidence suggests that impaired intestinal motility may facilitate gallstone formation by influencing biliary deoxycholate levels or by modulating interdigestive gall bladder motility (fig 2), although a primary intestinal defect in gallstone pathogenesis has not yet been demonstrated. In the cold war period, most interesting events, from a political point of view, occurred at the border between capitalist and communist systems, near the iron curtain. Similarly, the gall bladder and biliary tract can be viewed as the border between liver and intestinal tract, where many interesting things occur with profound impact on both systems. Combined efforts by researchers in the field of hepatology and gastrointestinal motility should brake down the Berlin wall of ignorance of one of the most common diseases in the Western world.

Background: The cholecystokinin provocation test (CCKPT) has been claimed to predict a better symptomatic result after cholecystectomy in patients with acalculous biliary pain., Aims: To examine the predictive value of the CCKPT for symptom relief after cholecystectomy in both CCKPT positive and negative patients., Patients and Methods: Fifty eight patients with acalculous biliary pain underwent CCKPT with serial ultrasound gall bladder volumetry. CCKPT positive patients were offered cholecystectomy; negative patients were reassessed and were offered a cholecystectomy if symptoms persisted. Six months after cholecystectomy, the CCKPT was repeated., Results: Of 32 CCKPT positive patients, 27 underwent cholecystectomy and of these, 18 (67%) became symptom-free. Postoperatively, 20 of 25 patients converted to CCKPT negative but five remained CCKPT positive and were symptomatic. Of the 26 CCKPT negative patients, nine became symptom-free without cholecystectomy; six of 14 (42.8%) patients undergoing cholecystectomy became asymptomatic and remained CCKPT negative. Cholecystectomy seemed to reduce symptoms in both groups, but there was no significant difference in the symptomatic outcome between preoperative CCKPT positive and negative patients., Conclusions: In this study, cholecystokinin provocation testing did not predict symptomatic benefit from cholecystectomy and we suggest it should no longer be used in the evaluation of patients with acalculous biliary pain.

Background and Aim: An impaired contractility has been suggested as a contributor to the increased incidence of gallstones in liver cirrhosis, but the few studies on gall bladder emptying in cirrhotics offered contradictory results. Ingestion of a meal triggers the physiological pathway of gall bladder emptying; therefore, it was decided to analyse postprandial kinetics by investigating simultaneously the rates of gastric and gall bladder emptying of a mixed meal in patients with liver cirrhosis., Methods: Gastric and gall bladder emptying were measured using ultrasound techniques after a solid-liquid meal (14 g fat, 425 kcal) in 24 patients with liver cirrhosis and in 12 controls. None of the subjects had gall bladder disease. Sequential changes in cross sectional area of the gastric antrum and in gall bladder volume were represented as a monoexponential process after the test meal. Cirrhotic patients were analysed according to the severity of disease (Child classes). The presence of portal gastropathy was assessed by endoscopy. Differences between groups were assessed using the two tailed Student's t test for unpaired observations and the correlations by linear regression (Pearson's coefficient)., Results: It was found that gastric emptying after the solid-liquid meal was delayed in cirrhotic patients compared with controls. Gall bladder emptying was significantly diminished in cirrhotic patients: the area under curve was greater in Child A (p = 0.01), Child B (p = 0.04), and Child C (p = 0.014) cirrhotics compared with controls. No correlation was found between the variables of gastric and gall bladder emptying. Gall bladder refilling began earlier in cirrhotics than in controls, before completion of gastric emptying., Conclusions: These results indicate the lack of coordination between gastric and gall bladder emptying in liver cirrhosis. They also support the hypothesis that diminished gall bladder contractility might contribute to the increased gallstone formation in liver cirrhosis.

To evaluate whether the extent of postprandial gall bladder emptying is correlated with gall bladder fasting volume, gall bladder motility was studied in 56 patients with cholesterol gall stone and 19 control patients. Gall bladder volumes were determined sonographically, while cholecystokinin plasma values were measured radioimmunologically. Twenty three per cent of gall stone patients were classified as pathological contractors (residual fraction > mean +2SD of controls) and 77% as normal contractors. Normal but not pathological contractor patients exhibited larger gall bladder fasting volumes (mean (SEM)) (24.7 (1.7) ml) than controls (15.3 (1.2) ml, p < 0.001). In normal contractor patients and controls fasting volume was closely related with ejection volume (r = 0.97, p < 0.001) and residual volume (r = 0.80, p < 0.001). Although ejection volume was enlarged in normal contractor patients it did not compensate the increase in fasting volume. Thus, residual volumes were considerably increased not only in pathological contractors (12.7 (2.5) ml, p < 0.001) but also in normal contractor patients (7.0 (0.5) v 4.6 (0.6) ml, p < 0.001). Postprandial cholecystokinin secretion did not differ between patients and controls. It is concluded, that in normal contractor patients gall bladder fasting volume is closely correlated with ejection and residual volume. Thus, fasting volume may be an essential factor affecting postprandial gall bladder emptying. Large fasting volumes in cholesterol gall stone disease could thereby contribute to bile retention, which facilitates gall stone growth.

Repeated daily injections of the somatostatin analogue, octreotide (SMS201-995, Sandostatin) are an effective treatment for acromegaly, but lead to gall stone formation in about 50% of cases during longterm treatment. This is probably because of impaired gall bladder contraction. This study examined whether the timing of intermittent injections in relation to meals, or alternatively, continuous 24 hour subcutaneous octreotide infusion (CSOI) might avert adverse effects on gall bladder contraction. In six patients with active acromegaly, gall bladder volume, plasma cholecystokinin (CCK), and pancreatic polypeptide (PP) were measured in the fasting state and after consumption of a fatty meal. Measurements were made on five separate days: (a) without treatment, (b) 45 minutes after 100 micrograms octreotide given subcutaneously, (c) four hours after 100 micrograms octreotide given subcutaneously, (d) eight hours after 100 micrograms octreotide given subcutaneously, and (e) during CSOI of 300 micrograms/24 h for two weeks. Without treatment, postprandial gall bladder contraction was 86.2 (2.1%). Fasting gall bladder volume increased after octreotide injection and was almost doubled during CSOI. Octreotide injections impaired postprandial gall bladder contraction as well as CCK and PP release for at least four hours. Eight hours after injection and during CSOI, postprandial gall bladder contraction was partly restored (43.4% and 50.8% respectively). Postprandial CCK release was normal at eight hours after injection but very low during CSOI. PP release was suppressed by each mode of octreotide treatment. This study indicates that octreotide injections impair postprandial gall bladder contraction for at least four hours. Eight hours after injection and during CSOI, gall bladder contraction is partly restored.

In this study gall bladder emptying patterns in response to a solid meal were studied using ultrasound. A similar triphasic pattern was seen in eight healthy control subjects and eight patients with gall stones, with 'early' and 'late' net emptying phases separated by a period of net refilling with peak postprandial gall bladder volumes occurring at (mean (SD)) 33.1 (17.9) minutes and 27.4 (18.8) minutes in control subjects and patients, respectively. A phase of slower net emptying followed, which was complete at 146 (33) minutes in control subjects and 125 (33) minutes in the gall stone patients (not significant). Superimposed upon this overall triphasic pattern, postprandial gall bladder emptying was punctuated by repeated short lived episodes of filling and emptying. The mean (SD) estimated postprandial bile outputs were 0.83 (0.34) ml/min in four control subjects and 1.2 (1.1) ml/min in seven patients with gall stones. We propose a 'washout' model to reconcile this large turnover of bile with the concentrating and storage functions of the gall bladder and predict that the extent rather than the rate of gall bladder emptying is important in determining stasis of bile in the gall bladder.