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PubMed1997

Pravastatin has no effect on bile lipid composition, nucleation time, and gallbladder motility in persons with normal levels of cholesterol.

Pravastatin dissolves gallstones in patients with hypercholesterolemia by reducing the cholesterol saturation index (CSI) of bile. There are few reports on effect of pravastatin on bile lipids, CSI and nucleation time (NT) in patients with gallstones and normal plasma lipid levels, or on the effect of pravastatin on gallbladder motility. Therefore we studied the effect of pravastatin on bile lipids, CSI, NT, and gallbladder motility in persons with normal cholesterol levels. We included 10 patients (ages 32 +/- 8 years; 6 men) with symptomatic gallstones and normal plasma lipid profiles. Estimation of bile lipids, CSI, and NT in duodenal bile and gallbladder motility were done using standard methods. Subsequently each patient was given 40 mg pravastatin daily for 1 month. At completion of pravastatin therapy, bile lipids and gallbladder motility studies were repeated. After pravastatin therapy, we found no significant reduction in bile cholesterol (11.2 +/- 3.2 vs. 10.4 +/- 2.8 mmol/l), bile acids (114.6 +/- 7.4 vs. 133 +/- 16 mmol/l), phospholipids (23 +/- 3.5 vs. 24 +/- 6.2 mmol/l), CSI (1.28 +/- 0.4 vs. 1.22 +/- 0.3), and nucleation time (7 +/- 3 vs. 7 +/- 3 days). In addition, there was no significant change in gallbladder fasting volume (26 +/- 3 vs. 26.6 +/- 3 ml), residual volume (14.6 +/- 1.1 vs. 15.08 +/- 1.4 ml), ejection fraction (44% vs. 43%), and rate constant of gallbladder emptying (0.018/min vs. 0.022/min). One-month therapy with pravastatin does not alter bile lipids, CSI, NT, and gallbladder contractility in persons with normal levels of cholesterol.

Adult↗
PubMed1999

Normal gallbladder ejection fraction after morphine augmentation.

PURPOSE: Morphine sulfate causes spasm of the sphincter of Oddi. Conversely, the cholecystagogue sincalide produces relaxation of the sphincter and contraction of the gallbladder. This prospective study evaluated whether sincalide could produce normal gallbladder emptying after low-dose morphine sulfate (0.04 mg/kg). METHODS: Thirty to 120 minutes (mean, 51 minutes) after morphine sulfate-augmented gallbladder visualization, 25 gallbladder ejection fractions in 24 patients were measured. One patient was studied twice, 2 weeks apart. Gallbladder ejection fractions were calculated after controlled 30-minute infusions of sincalide (0.02 microg/kg). RESULTS: Fourteen gallbladder ejection fractions were normal (mean, 63%; range, 45% to 80%) and 11 gallbladder ejection fractions were abnormal (mean, 12%; range, 5% to 19%; P < 0.001). CONCLUSIONS: Normal gallbladder ejection fractions can be obtained as early as 30 minutes after administration of low-dose morphine sulfate. Potential applications of post-morphine sulfate sincalide challenge would include, for example, to support true-negative morphine sulfate-augmented gallbladder visualization in a patient with a high clinically indicated potential of having acute cholecystitis.

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↗
PubMedDate not supplied

Effect of bile salts on in vitro gallbladder motility: preliminary study.

Impaired postprandial gallbladder emptying may be an important factor in cholesterol crystals precipitation and subsequent gallstone formation. We previously found strongly increased bile salt concentrations in gallbladder bile of gallstone patients with weak (< 50% fasting volume) postprandial gallbladder contraction compared to patients with strong (> 50%) postprandial contraction. Therefore, we studied potential effects of various conjugated and unconjugated bile salts with different relative hydrophobicity on in vitro contractility of gallbladder muscle strips obtained at cholecystectomy. Strips were incubated 5 min with bile salt at concentrations of 10(-8)-10(-4)M. The effect of 10(-3)M acetylcholine was measured and related to preincubation control value. Bile salts used were, in order of increasing hydrophobicity: tauroursodeoxy-, ursodeoxy-, tauro-, taurodeoxy- and deoxycholate. Ursodeoxy- and tauroursodeoxycholate did not significantly reduce gallbladder contractility. Taurocholate significantly reduced contractility at concentrations of 10(-6) M and higher, taurodeoxycholate at 10(-7) M and higher and deoxycholate at 10(-5) M and higher. Contractility induced by acetylcholine 10(-3) M at a bile salt concentration of 10(-4) M was 66.0 +/- 11.7% (taurocholate), 50.2 +/- 6.2% (deoxycholate) and 44.8 +/- 11.5% (taurodeoxycholate) of control. The effect of bile salts correlated with their relative hydrophobicity (r = -0.97; p < 0.01). Suppressing effects on gallbladder muscle strip contractility were long lasting and remained after rinsing. Results show that bile salts in the physiological dose range inhibit in vitro gallbladder contraction. If this mechanism exists in vivo, it may have important implications for gallbladder motility regulation.

Acetylcholine↗
PubMed1984

[Gallbladder sludge: a sonographically recognizable stage of lithogenesis].

The appearance and the natural course of gallbladder sludge were studied by ultrasonography in 82 patients. Sludge was found in conditions with a functional or organic disturbance of gallbladder emptying: alcoholic cirrhosis and an atonic gallbladder in the fasting state, e.g., extrahepatic ductal obstruction and obstruction of the cystic duct. No clinical complaints could be attributed to sludge. After the normal bile flow had re-established the sludge disappeared in many cases. In 9 of 82 sludge-positive patients (10,9 per cent) ultrasonography revealed gallstone formation. Newly-formed stones obtained from 2 patients had the aspect of pigment stones and were analyzed by infrared spectroscopy. They consisted of calcium bilirubinate. This material constitutes the pigment granules which are suspended in the sludge. It was concluded that sludge was an early phase of stone formation. Alcoholic cirrhosis, obstruction of the biliary tract, gastrectomy, celiac sprue and prolonged fasting may predispose to lithiasis secondary to the precipitation of sludge in a large, atonic or distended gallbladder. Ultrasonography is instrumental to detect an early state of gallstone formation in those patients who carry a risk.

Cholelithiasis↗
PubMed2000

Acute intraduodenal bile salt depletion leads to strong gallbladder contraction, altered antroduodenal motility and high plasma motilin levels in humans.

Cholecystokinin is the main hormone involved in postprandial gallbladder contraction. There is also considerable gallbladder contraction in the fasting state, associated with phase III of the gastrointestinal migrating motor complex and release of the hormone motilin. It has been proposed that intraduodenal bile salts exert a negative-feedback control on postprandial cholecystokinin release and resulting gallbladder contraction. We wanted to elucidate whether a similar control mechanism on gallbladder contraction exists in the fasting state. We therefore performed gallbladder ultrasonography and 24-h antroduodenal motility registrations and determined plasma cholecystokinin and motilin levels in six healthy subjects before and after acute (4 g) and chronic (8 days; 8 g day(-1)) oral cholestyramine. Acute cholestyramine strongly decreased gallbladder volumes and increased motilin without changed cholecystokinin levels. There was a negative relationship between gallbladder volumes and plasma motilin levels. Although there was a persistent fasting pattern of antroduodenal motility, its cycle length was increased (P < 0.03) with markedly longer phase II (P < 0. 005). Fasting gallbladder volumes 24 h later were still strongly decreased but gradually increased to pretreatment levels. Before and after 8 days cholestyramine, interdigestive and postprandial gallbladder emptying, intestinal migrating motor complex and hormone levels did not differ. We conclude that acute (but not chronic) intraduodenal bile salt depletion with cholestyramine affects gallbladder and antroduodenal motility, possibly partly related to motilin release.

Adult↗
PubMed1993

Abnormal gallbladder function in patients with irritable bowel syndrome.

Abnormalities of the autonomic nervous system function and cholecystokinin release have been described in patients with irritable bowel syndrome. Because the autonomic nervous system and cholecystokinin have an important role in the normal functioning of the gallbladder, we studied gallbladder contraction in response to a meal, using real time ultrasonography in irritable bowel syndrome patients (n = 20) and healthy controls (n = 15). The following parameters were studied: 1) fasting gallbladder volume, 2) residual volume after maximal contraction and at the end of 2 h, 3) maximum percent of gallbladder emptied, and 4) the time taken for maximal contraction. Fasting gallbladder volume (26.21 +/- 1.81 ml vs 15.21 +/- 1.63 ml, p < 0.001), and residual volume after maximal contraction (14.2 +/- 1.69 ml vs. 5.86 +/- 0.98 ml, p < 0.001) and at the end of 2 h (18.81 +/- 1.73 ml vs. 11.65 +/- 1.45 ml, p < 0.01) were significantly higher in the patient group, compared with controls. The maximum emptying was less (49.55 +/- 2.75% vs. 63.98 +/- 4.55%, p < 0.01) and the time taken for maximal contraction (59.25 +/- 3.8 min vs. 42.33 +/- 2.04 min, p < 0.001) was longer in the patient group than in the controls. Based on these observations, we conclude that patients with irritable bowel syndrome have significant abnormalities of gallbladder motor function.

Adolescent↗
PubMed2000

Effects of very long chain versus long chain triglycerides on gastrointestinal motility and hormone release in humans.

Fish oil (a very long chain triglycerides, VLCT) has received much attention because of its favorable metabolic properties; however, its effect on gastrointestinal function has not been studied. We investigated the effects of intraduodenally administered VLCT on gut-hormone release [cholecystokinin (CCK), neurotensin, peptide YY (PYY)], gallbladder emptying, antroduodenal motility, and small bowel transit time (SBTT) in comparison to intraduodenal administration of saline and long chain triglycerides (LCT, corn oil) in nine healthy volunteers. Gallbladder contraction duration was significantly shorter after VLCT than after LCT (138 +/- 16 min vs 233 +/- 38 min, P < 0.05). Both fats induced a fed motility pattern, while SBTT was not significantly altered. CCK secretion was significantly reduced after VLCT compared to LCT (36 +/- 12 pM x 120 min vs 78 +/- 15 pM x 120 min, P < 0.05), whereas PYY and neurotensin release were not significantly different. In conclusion, effects of triglycerides on CCK and gallbladder motility appear to be chain-length dependent, in contrast to the effects on distal gut-hormone release and intestinal motility and transit, which appear to be chain-length independent.

Adolescent↗
PubMed1992

Early stages of gallstone formation in guinea pig are associated with decreased biliary sensitivity to cholecystokinin.

The purpose of this study was to measure differences in gallbladder sensitivity to cholecystokinin (CCK) in vivo during the early stages of gallstone formation and to correlate these findings to gallbladder CCK receptors. Guinea pigs were placed on either a normal diet or a two-week cholelithogenic diet, after which gallbladder emptying pressure to exogenously administered CCK was measured in vivo, according to the presence or absence of gallstones. At all doses of CCK tested (except 10(-10) mol/kg), the gallbladder response to CCK of guinea pigs that did not develop gallstones (on the cholelithogenic diet) was more sensitive than that of guinea pigs that did develop gallstones. Neither group was different from guinea pigs on a normal diet. In a second experiment, CCK receptors were measured on gallbladder muscularis from guinea pigs after two weeks on the same diet as in the first experiment. Those guinea pigs that did not develop gallstones had greater concentrations of CCK receptors (149 +/- 9 fmol/mg protein) than those that did develop gallstones (70 +/- 23 fmol/mg protein). Neither group was different from normal diet guinea pigs (119 +/- 57 fmol/mg protein). At the time point measured, there were no differences in the lipid chemistry or protein concentrations of gallbladder bile between the guinea pigs on the cholelithogenic diet that did or did not develop gallstones, or those on normal guinea pig chow. We conclude that the early stages of gallstone formation in guinea pigs are associated with decreased gallbladder sensitivity to CCK and that this change may be due to a lower concentration of CCK receptors on the gallbladder smooth muscle.

Animals↗
PubMedDate not supplied

Direct inhibitory effect of erythromycin on the gallbladder muscle.

Erythromycin, a macrolide antibiotic, stimulates motor activity in various parts of the gastrointestinal tract in humans and animals. This effect of erythromycin resembles that of motilin, a gastrointestinal hormone, in evoking contractions similar to phase 3 activity of the migrating motor complex. Motilin induces contractions in the canine gallbladder but fails to evoke any response, either in vivo or in vitro, in the human gallbladder. Surprisingly, erythromycin stimulates human gallbladder emptying in healthy volunteers and in persons with diabetic autonomic neuropathy. In the present study we examined the effect of erythromycin on chemically and electrically evoked contractions of isolated gallbladders from guinea pigs and humans by use of isometric force measurements. Carbachol, a muscarinic cholinergic agonist, evoked gallbladder contractions that were diminished by erythromycin in a concentration-dependent manner: at 200 micromol/L the contractions were 86% +/- 20% of the control response, at 500 micromol/L they were 63% +/- 21% of control, and at 1000 micromol/L they were 41% +/- 20% of control (P <0.05, N = 10, mean +/- standard deviation). Electrically evoked gallbladder contractions were reduced to 68% +/- 18% of the control response with the addition of 500 micromol/L of erythromycin and to 56% +/- 19% of control after the addition of 1000 micromol/L (P <0.05, N = 8). Guinea pig but not human gallbladders contracted after stimulation with the alpha-adrenergic agonist phenylephrine. Erythromycin reduced these contractions in a concentration-dependent manner but had no effect on gallbladder contractions induced by bradykinin. In human gallbladder strips, erythromycin at 500 micromol/L reduced the contractile response to electrical stimulation to 71% +/- 16% of the control value (N = 10 [5 patients], P <0.01) and the carbachol-evoked contractions to 53% +/- 24% (P <0.01, N = 32). The inhibitory effect of erythromycin persisted in the presence of the nerve blocker tetrodotoxin at 1 micromol/L. It is concluded that erythromycin has a direct inhibitory effect on guinea pig and human gallbladder contractions.

Adrenergic alpha-Agonists↗
PubMed1992

Dose-response effects of oral loxiglumide on postprandial gall-bladder emptying in man.

The effect of two different single oral doses of loxiglumide (CR 1505, CAS 107097-80-3) on gall-bladder emptying induced by a 550-cal standard mixed meal in 6 healthy volunteers was studied. Following placebo, the maximal gall-bladder emptying occurred about 90 min after the meal (minimal residual gall-bladder volume 27.4% of basal volume). Loxiglumide 400 or 800 mg dose-dependently inhibited the physiologica gall-bladder emptying. Loxiglumide plasma levels dose-dependently increased. The inhibition of gall-bladder emptying and the kinetic of loxiglumide plasma levels were temporally related. The results of the present study confirm that oral loxiglumide is a potent orally active cholecystokinin (CCK) antagonist in man and that CCK is the major physiological mediator of gallbladder emptying in response to meal.

Adult↗
PubMed2002

Effects of ileal bile salts on fasting small intestinal and gallbladder motility.

In the fasting state, gallbladder emptying is related to phase III of the intestinal migrating motor complex. The effects of ileal infusion of mixed taurocholate-phospholipid micelles on fasting small intestinal motility (by a 17-channel catheter with side holes located in duodenum, jejunum and ileum) and gallbladder motility (by ultrasound) were investigated in eight healthy volunteers. After bile salt depletion by cholestyramine, 0.9% NaCl or mixed micelles were infused in the ileum during phase II of the migrating motor complex. Time to onset of subsequent phase III was significantly shorter after infusion of mixed micelles compared with 0.9% NaCl (32 +/- 5 min vs. 60 +/- 5 min, P = 0.01). Distal to the infusion port, numbers of pressure waves and their amplitudes were significantly lower during bile salt infusion compared with 15 min before infusion (11 +/- 6 per 15 min vs. 21 +/- 8 per 15 min, and 2.4 +/- 0.6 kPa vs. 2.8 +/- 0.5 kPa, respectively). Micellar infusions increased fasting gallbladder volumes to 170 +/- 5% of starting volumes (P < 0.0001). In conclusion, ileal infusion of mixed micelles influences the timing of phase III of the intestinal migrating motor complex, inhibits ileal motility and increases fasting gallbladder volumes. These findings may have important consequences for enterohepatic circulation of bile salts.

Adult↗
PubMed2002

Effect of nitric oxide on gallbladder motility in patients with acalculous biliary pain: a cholescintigraphic study.

The aim of the present study was to evaluate the influence of the exogenous nitric oxide donor glyceryl trinitrate on cerulein-induced gallbladder contraction in patients with acalculous biliary pain. Quantitative hepatobiliary scintigraphy was performed on 33 patients. From the 60th min cerulein (1 ng/kg body wt/min for 10 min intravenous) then from the 90th min the same dose of cerulein plus glyceryl trinitrate (0.5 mg sublingually) (21 patients) or placebo (12 patients) were administered and the gallbladder ejection fraction was measured repeatedly. After the first dose of caerulein, the gallbladder ejection fraction was less than 35% in 23 of 33 patients (nonresponders), while it was more than 35% in the remaining 10 patients (responders). After the second dose of cerulein in 16 nonresponder patients glyceryl trinitrate administration significantly increased the previously impaired gallbladder ejection fraction while in 7 nonresponder patients placebo administration had no effect. In conclusion, normalization of the gallbladder ejection fraction in the majority of patients following glyceryl trinitrate administration suggests that impairment of gallbladder emptying is caused by a functional motility disorder rather than any organic disease.

Biliary Dyskinesia↗
PubMed1996

Gallbladder motility in systemic sclerosis.

In 20 patients with systemic sclerosis (SSc) and 24 healthy controls, gallbladder motility was evaluated by abdominal ultrasonography after stimulation by a standard liquid meal. Results from patients with normal and disturbed oesophageal function were analysed separately in order to investigate the significance of gallbladder motility as a parameter for gastrointestinal involvement in SSc. All patients showed a marked decrease in gallbladder size after stimulation (patients 61 +/- 13%; controls 48 +/- 12%). Patients with oesophageal dysfunction (n = 12) had a slightly lower gallbladder contraction (maximal decrease = 58 +/- 13%) when compared to patients with normal oesophageal function (n = 8; 66 +/- 13%); however, this difference was not statistically significant. Gallbladder motility in patients with SSc was not reduced when compared with healthy controls. SSc-induced oesophageal dysfunction was not associated with impaired gallbladder motility. Thus, measurement of gallbladder emptying is not a helpful tool when looking for gastrointestinal involvement in SSc.

Adolescent↗
PubMed2005

Gallbladder contraction, gastric emptying and antral motility: single visit assessment of upper GI function in untreated celiac disease using echo-planar MRI.

PURPOSE: To assess gallbladder contraction, gastric emptying, and antral motility in untreated celiac patients and healthy controls using a single MRI examination. MATERIALS AND METHODS: Gallbladder emptying, gastric emptying, and antral motility were measured in 15 celiac patients and 15 age/sex-matched healthy controls following a 323-kcal test meal using EPI techniques. Postprandial dyspepsia scores were recorded on a questionnaire. RESULTS: Fasting gallbladder volume (P=0.01) and the volume of bile ejected postprandially (P=0.014) were increased in celiacs. Gastric emptying tended to be slower in celiacs (P=0.142). Three celiac patients with severe postprandial dyspepsia and total villous atrophy had pathologically delayed gastric emptying and increased fasting gallbladder volume. Antral contractions were absent in five out of 14 patients (36%) five minutes after the meal, but in none of 10 volunteers in whom the antrum could be visualized (P=0.128). CONCLUSION: This study shows that using MRI, multiple parameters related to upper gastrointestinal function in celiac disease can be measured in a single noninvasive study, whereas previously three separate visits would have been required. Celiacs have increased fasting gallbladder volumes and tend to have slower gastric emptying.

Adolescent↗
PubMed2003

Motility and dysmotility of the biliary tract.

Muscle fibers in the biliary tree, and therefore the potential for dysmotility, are located in the gallbladder and the sphincter of Oddi. Dysmotility at either site is a potential cause of biliary pain in the absence of stones, although significant controversy persists. Diminished gallbladder emptying measured by biliary scintigraphy is an indication for cholecystectomy, although studies are contradictory regarding clinical benefit. It is likely that careful selection of patients for cholescintigraphic testing, many of whom have had missed stones or sludge, will identify patients who benefit from cholecystectomy. However, given the increased incidence of gallbladder stasis in functional gastrointestinal disorders, wide use of this study in patients with abdominal symptoms leads to a frequent failure to respond to cholecystectomy. Sphincter of Oddi dysfunction (SOD) has been best studied in patients with biliary type pain who have had prior cholecystectomy. Much less understood is the association of SOD with idiopathic recurrent acute pancreatitis and chronic pancreatitis. The least-studied clinical association for SOD is in patients with biliary pain and intact gallbladders. Elevated basal sphincter of Oddi pressure is predictive of clinical response to sphincterotomy in patients with postcholecystectomy pain in two randomized sham-controlled studies. However, patients with suspected SOD have the highest complication rate from endoscopic retrograde cholangiogram and sphincterotomy, and, therefore, careful patient selection is mandatory.

Adult↗
PubMed2000

Evidence of impaired gallbladder function in patients with liver cirrhosis by quantitative radionuclide cholescintigraphy.

OBJECTIVE: The aim of this study was to understand gallbladder function in liver cirrhosis. METHODS: Gallbladder function was measured in 45 patients with liver cirrhosis by Tc-99m-labeled imino-diacetic acid analog cholescintigraphy. Gallbladder function was represented by the filling fraction and the ejection fraction (EF). The patients were divided into three groups, based on cirrhotic severity, using the modified Child's classification: A = good, B = fair, and C = poor. Fifteen normal control subjects were selected for comparison. RESULTS: There were no significant differences in filling fraction among all of the study groups. Normal controls had significantly higher 60-min EF values than did liver cirrhosis patients. Among the liver cirrhosis patients, class A patients had the highest EF values, and class C patients had the lowest EF values. CONCLUSIONS: We found that liver cirrhosis may significantly impair the gallbladder emptying, based on the evidence of quantitative Tc-99m-labeled imino-diacetic acid analog cholescintigraphy findings.

Female↗