Effect of nifedipine on interdigestive gallbladder volume and postprandial gallbladder emptying in man

The effect of two oral doses (10 and 20 mg) of nifedipine versus placebo on the fasted gallbladder volume and on the meal-induced gallbladder emptying was assessed according to a double-blind study protocol in 12 healthy volunteers. Eight subjects underwent three studies (with placebo and with both nifedipine doses), whereas in two subjects the effect of a 10-mg nifedipine dose, vs placebo and in two others the effect of a 20-mg nifedipine dose vs placebo was examined. The studies were performed on separate days, and the gallbladder volume was measured by means of real-time ultrasonography. Neither placebo nor 20 mg nifedipine per os elicited any significant change in the fasted gallbladder vlume. With 10 mg nifedipine per os a significant increase in the interdigestive gallbladder volume was observed: 22.9±2.9 cm³ before and 26.2±3.2 cm³ after the drug receipt (P<0.005). A trend towards an inhibition of the postprandial gallbladder emptying was observed with 10 mg nifedipineper os without, however, reaching the level of statistical significance. Following 20 mg nifedipineper os, a marked delay in the meal-stimulated gallbladder emptying occurred as reflected by a decrease in the gallbladder ejection fraction from 48.1±4.5% (placebo) to 26.4±5.0% (nifedipine) (P<0.02) at 30 min and from 54.0±3.6% (placebo) to 33.2±4.6% (nifedipine) (P<0.02) at 40 min after the test meal. We conclude that a therapeutic oral dosage of nifedipine has a significant relaxing effect on the human gallbladder.     

Gall Bladder Emptying in Patients with Corrosive-Induced Esophageal Strictures

Ingestion of corrosive substances can lead to strictures of the esophagus and stomach. Cicatrization of the lower part of the esophagus can entrap vagal fibers in the process of fibrosis. The aim of the present study was to evaluate gallbladder dysfunction as a sequel to vagal damage in patients with corrosive-induced esophageal strictures. The cephalic phase of gallbladder emptying was stimulated by modified sham feeding according to the chew-and-spit method. Gallbladder volume was measured by ultrasonography using the ellipsoid method after an overnight fast and every 15 min for a period of 90 min after sham feeding in 22 patients and 10 controls. Mean fasting gallbladder volume was significantly greater in patients than in controls (22.09± 9.78 vs. 14.61± 4.42 ml; P = 0.025). After sham feeding the gallbladder ejection fraction was significantly lower in patients than in controls (32.86± 17.21 vs. 49.40± 7.86%; P = 0.007). Patients with cicatrization in the distal one-third of the esophagus had a greater basal gallbladder volume (24.57± 9.2 ml) and significantly lower ejection fraction (20.47± 8.9%) than patients with strictures at other sites (gallbladder volume, 18.50± 10.69 ml; ejection fraction, 47.48± 13.3%; P = 0.001). In conclusion, patients with corrosive-induced esophageal strictures, especially those in the distal one-third, had an increased fasting gallbladder volume and decreased cephalic phase of gallbladder emptying, pointing to impaired vagal cholinergic transmission, possibly due to vagal entrapment in the cicatrization process.     

Oral administration of loxiglumide (CCK antagonist) inhibits postprandial gallbladder contraction without affecting gastric emptying

The effect of a single oral dose of loxiglumide, a cholecystokinin antagonist, on postprandial gallbladder contraction and on gastric emptying was evaluated in humans. Following a 12-hr fasting period, two tablets of loxiglumide (400 mg each) or placebo was administered on different days, in random order and in a double-blind fashion to 10 healthy volunteers 15 min before the ingestion of a 1050-kcal standard meal. Gallbladder and antral volumes were measured by real-time ultrasonography in basal conditions and at fixed time intervals after the meal. Oral loxiglumide administration was followed by a total inhibition of the gallbladder contraction for 60 min after the end of the meal ingestion. Thereafter, up to the end of the study period, gallbladder volume was larger than that of the placebo study (at 300 min after the meal 2.7±1.6 ml after placebo and 8.2±3.5 ml after loxiglumide; P<0.008). No difference between placebo and loxiglumide was found in the antral volumes at any time interval (postprandial 63.5±16.5 ml after placebo and 59.4±24 ml after loxiglumide; at 300 min after the meal 20.8±13.3 ml after placebo and 18.9±9.5 ml after loxiglumide). In conclusion, a single oral dose of loxiglumide at the dose of 800 mg can inhibit postprandial gallbladder contraction without affecting gastric emptying. It would therefore appear that in man endogenous CCK, released after a solid-liquid, caloric, nutrient-balanced meal, plays a major role in the contraction of the gallbladder but does not affect gastric emptying.     

Gallbladder Fasting Volume Is Reduced and Gallbladder Postprandial Emptying Is Enhanced by Intravenous Erythromycin

It has been recently shown that erythromycin, amacrolide antibiotic, exhibits prokinetic properties, byenhancing gastric emptying in health and disease and byinducing gallbladder contraction. The aim of the study was to further investigate theeffect of intravenous erythromycin on gallbladdermotility during fasting and postprandial states. In 10healthy male subjects gallbladder emptying was assessed by ultrasonography on three differentoccasions, each in a random sequence, as follows: (1)after giving 300 ml of fresh milk and infusing normalsaline as placebo (postprandial emptying), (2) afterinfusing 200 mg of erythromycin during the fastingstate, and (3) after infusing 200 mg of erythromycinalong with ingestion of 300 ml of fresh milk. Infusionof erythromycin and placebo lasted 10 min. From the emptying curves, the duration of the lag phaseof emptying, the ejection fraction of emptying, and thetime by which maximal emptying was achieved werecalculated. Infusion of erythromycin induced animmediate contraction [lag phase (±SD): 1.3± 2.6 SD min] of the gallbladder by 42.1 ±22% of its initial volume. Infusion of erythromycinduring the postprandial state significantly decreasedthe duration of the lag phase (1.3 ± 3.5 min after erythromycinplus test meal versus 3.6 ± 4.2 min after testmeal only, P < 0.04) and significantly increased theejection fraction (78 ± 8.5% after erythromycinplus test meal versus 60.6 ± 8.5% after test meal only, P <0.0008). It is concluded that intravenously givenerythromycin induces contraction of the gallbladderduring the fasting state and enhances postprandialgallbladder emptying by accelerating the initiation and increasingthe extent of emptying.     

Effect of aspirin on gallbladder motility in patients with gallstone disease

Patients with gallstone disease have impaired gallbladder motility. Prostaglandins are thought to be important mediators of gallbladder hypomotility. We assessed the effect of aspirin, a prostaglandin inhibitor on gallbladder resting volume and ejection fraction according to a double-blind study protocol in 20 healthy volunteers and 30 patients with gallstone disease. Healthy volunteers had a higher ejection fraction compared to patients with gallstone disease (73.9±0.9% vs 60.4±1.0%,P<0.05). Aspirin in a dose of 350 mg/day for two weeks did not alter gallbladder motility in the healthy volunteers. Thirty patients with gallstone disease were randomized into three treatment groups: group I (placebo), group II (aspirin 350 mg/day), and group III (aspirin 1400 mg/day). After two weeks of treatment, gallbladder ejection fraction was improved in group II (74.0±1.7% vs 62.0±1.7%,P<0.01) and group III (69.8±3.8% vs 61.2±1.3%,P<0.01) but not in group I (60.4±2.6% vs 59.0±1.9%,P=NS). The higher dose of aspirin did not induce a greater increase in gallbladder emptying. It is concluded that impaired gallbladder motility in patients with gallstone disease is corrected by short-term oral aspirin even in low dosage. This may be clinically useful in secondary prophylaxis after nonsurgical therapy for gallstone disease.     

Effect of extracorporeal shock-wave lithotripsy on gallbladder emptying in patients with solitary and multiple gallbladder stones

In a prospective study, we investigated the effect of extracorporeal shock-wave lithotripsy (ESWL) on gallbladder contractility and on fasting and residual gallbladder volume in patients with solitary and multiple gallbladder stones with stone densities<100 Hounsfield units (HU) and adequate gallbladder function. Twenty-five patients (seven males and 18 females, mean age 48.5±11.7 years) treated with ESWL were assigned to either group I, consisting of 13 patients with solitary stones<20 mm diameter, or group II, including patients with two to three stones and maximum stone diameter of 30 mm. ESWL was performed with the MPL 9000 lithotripter. Gallbladder ejection fraction was determined using the method of Dodds after a 12-hr fast and following application of a standard stimulative meal. Gallbladder volume was measured by ultrasound over 90 min at 10-min intervals before ESWL, then at 1, 30, 120, and 210 days after ESWL. At 24 hr after ESWL, residual gallbladder volume increased in group I from 7.4 ml to 13.9 ml (P=0.0567) and in group II from 6.5 ml to 20.2 ml (P=0.0076). Thereafter, residual volumes returned to pre-ESWL levels. In group II, post-ESWL fasting volumes were significantly increased over initial values at all time intervals. Correspondingly, only at 24 hr after ESWL, ejection fractions decreased from 73.1% to 64.9% in group I and from 76.5% to 62.7% in group II. No statistically significant differences in gallbladder contractility between the two groups were observed at any point of the follow-up period. ESWL exerts a no more than transient effect on gallbladder motility, regardless of stone count prior to ESWL. We postulate that changes in residual gallbladder volume and reductions in ejection fraction may be due to transitory disturbances in the gallbladder epithelium and resultant gallbladder wall edema.     

Role of nutrient fat and cholecystokinin in regulation of gallbladder emptying in man

Postprandial gallbladder contraction is mainly regulated by cholecystokinin (CCK), but little is known about the dose-response relationship between CCK release and gallbladder contraction, in particular after meals with differing fat content. Decreased postprandial gallbladder emptying has been suggested to play a major role in the development of gallstones in man, and dietary factors may therefore be important in the pathogenesis of gallbladder stasis. We studied, in a randomized order, the effect of three isocaloric meals (250 ml) with identical osmolality on CCK release and gallbladder contraction in six healthy volunteers: (1) a pure fat meal (25 g triglycerides); (2) a mixed meal containing fat (8 g, 29% of caloric content), protein (10 g, 17%), and dextrose (32 g, 54%); and (3) a fat-free meal containing albumin (25 g, 46%) and dextrose (32 g, 54%). Gallbladder volumes and antral cross-sectional areas were determined by ultrasonography and plasma CCK and PP levels by RIA. The pure fat meal caused the highest CCK release (187±27; mean ±sem) and maximal (>85% of fasting volume) gallbladder contraction (3172±361; AUC) as compared to the other two meals (P<0.05). The mixed and the fat-free meal caused similarly low (<50% of fasting volume) gallbladder contraction (6052±342 and 6134±500, respectively), although they induced markedly different CCK levels (157±12 and 87±13, respectively;P<0.05). Gastric emptying rates were similar for all meals (18,500±3300, 18,600±2700 and 19,800±3100, respectively). The results of this study suggest that CCK plays a major role in the stimulation of gallbladder contraction but that other factors besides CCK are implied when fat-free or low-fat meals are ingested. Furthermore, our findings suggest that a fat intake of 25 g induces maximal gallbladder contraction and may thus prevent an understimulation of gallbladder contraction and the formation of gallbladder stones.     

Gallbladder emptying,plasma levels of estradiol and progesterone,and cholecystokinin secretion in liver cirrhosis

Defective gallbladder emptying has been proposed as a possible accessory pathogenetic factor to explain the increased prevalence of gallstones in liver cirrhosis. In this study we have evaluated the fasting volume and the meal-stimulated emptying of the gallbladder, the plasma levels of estradiol and progesterone, and the basal and postprandial secretion of cholecystokinin in Child A cirrhotic patients compared to normal subjects. Basal (42.2±27 vs 22.8±8.4 ml) (P<0.002) and residual (8.4±8.7 vs 4.6±3.8 ml) (P<0.05) gallbladder volumes were higher in cirrhotics but neither the integrated gallbladder response to meal nor the maximal percentage of emptying was significantly different. Circulating estradiol and progesterone was slightly increased in only 1/13 and 5/13 cirrhotics, respectively. In eight cirrhotics and seven normals taken from the overall populations, the secretion of cholecystokinin was also measured. The fasting plasma level of cholecystokinin was higher in the cirrhotics (6.71±5.08 vs 2.02±0.46 pmol/liter) (P<0.01). The meal-stimulated integrated plasma cholecystokinin response also was greater in cirrhotics (438.5±615 pmol/liter/270 min) than in normals (153±170.4 pmol/liter/270 min), but this difference was not significant because of the small study population. In spite of a normal kinetics of postprandial emptying, cirrhotic patients show increased fasting gallbladder volume and increased plasma levels of basal and postprandial cholecystokinin. Circulating estradiol and progesterone do not seem to be responsible for the large gallbladder volume found in liver cirrhosis.     

Effect of erythromycin on gallbladder emptying in diabetic patients with and without autonomic neuropathy and high levels of motilin

A reduction of gallbladder emptying in response to neural or hormonal stimulation has been reported in patients with diabetes mellitus. Decreased gallbladder emptying may be a key factor in the pathogenesis of gallbladder stones. Few drugs, if any, are able to stimulate gallbladder emptying. However, in a previous study we demonstrated that erythromycin, a macrolide antibiotic, stimulates gallbladder emptying and motilin release in healthy human subjects by an atropine-sensitive pathway. Therefore, the present study was designed to evaluate the effect of erythromycin on gallbladder emptying and motilin release in diabetic patients with or without cardiac autonomic neuropathy (AN). Thirteen diabetic patients, six with AN, and 10 healthy subjects were enrolled in the study protocol. Gallbladder emptying was determined by sonography after ingestion of a standard meal and during infusion of erythromycin alone or together with 6 g/kg/hr atropine. We found that 100 mg/hr erythromycin caused a significant reduction in gallbladder volume in both healthy subjects and diabetic patients. The ejection fraction (mean ±se) of 45.3±8.2% and 37.3±5.0% was similar. The presence of AN had no influence on gallbladder emptying induced by erythromycin. Basal motilin plasma levels were 111.5±14.5 pmol/liter in diabetic patients and 63.3 ±6.0 pmol/liter in healthy subjects (P<0.01). However, patients with AN had higher (130.0 ±11.9 pmol/liter) motilin plasma levels than patients without (74.0±9.4 pmol/liter,P<0.01). Erythromycin administration caused an approximately twofold increase in plasma motilin concentrations in healthy subject and patients withou AN, but did not stimulate motilin release in neuropathic patients. A negative correlation (r=–0.75,P<0.01) was found between basal plasma levels of motilin and peak of gallbladder emptying induced by erythromycin. Atropine completely inhibited the effects of erythromycin on gallbladder emptying and motilin release (P<0.001 by ANOVA). A negative correlation (r=–0.52,P<0.05) was also found between plasma glucose concentrations and peak of gallbladder emptying. Present results demonstrate that erythromycin could be used for treating alterations of gallbladder emptying in diabetic patients with or without AN.     

Severely impaired postprandial gallbladder emptying despite unchanged cholecystokinin release in the early phase of biliary colic

In the present article we report transitory severely impaired postprandial gallbladder emptying preceding biliary colic in a cholesterol gallstone patient. Gallbladder emptying 1 wk before and 3 wk after the biliary colic was normal. Treatment with ursodeoxycholic acid led to increased fasting gallbladder volumes, but the postprandial residual volume did not change. Postprandial cholecystokinin release appeared not to change during ursodeoxycholic acid treatment or during biliary colic.     

Increased Gallbladder Residual Volume in Nonresponders to Extracorporeal Shock Wave Lithotripsy of Gallbladder Stones

In a prospective study of 63 patients, we purposed to determine whether gallbladder contractility or gallbladder volume before biliary lithotripsy are predictors of fragment disappearance. Percentage gallbladder contraction was calculated from the fractional difference in the sonographically measured gallbladder volume after a standard fatty meal. Statistical analysis showed no significant differences in gallbladder contractility between the fragment-free group and the residual-fragment group before (77.2 +/- 12.7% vs. 71.9 +/- 19.3%; p = 0.1044) biliary lithotripsy and after the termination of adjuvant cholelitholysis therapy (76.4 +/- 12.9% vs. 72.2 +/- 17.1%; p = 0.1341). Before treatment, there was no significant difference in fasting gallbladder volume in either group (29.9 +/- 15.4 ml vs. 36.6 +/- 18.8; p = 0.0682), but postprandial gallbladder volume was greater in nonresponders (10.4 +/- 9.4 ml vs. 6.5 +/- 3.8; p = 0.0164). After termination of the therapy, both the fasting gallbladder volume (41.2 +/- 24.2 ml vs. 29.8 +/- 10.3 ml; p = 0.0093) and the postprandial gallbladder volume (11.9 +/- 11.7 ml vs. 7.3 +/- 5.3 ml; p = 0.0267) were greater in the residual-fragment group. The increase of the fasting gallbladder volume in the residual-fragment group was statistically not significant. Our results indicate that the increased residual volume is a significant cause of therapeutic failure in nonresponders.     

Noninvasive evaluation of kinetics of gallbladder emptying and filling in the dog

Patterns of gallbladder contraction induced by a meal or cerulein were examined by means of real-time ultrasonography in conscious dogs. The postprandial gallbladder emptying was characterized by two parameters of the power-exponential function: the gallbladder half emptying timeT1/2=47.3 ± 4.7 min and the curve shape paremeterS=0.866 ± 0.036. Cerulein infused at stepwise increasing rates of 0.7, 2.2, 7.4, 22.2, and 66.5 pmol/kg/hr, administered each for 10 min, evoked a gallbladder contraction to 87.4 ± 3.8%, 66.7 ± 2.4%, 44.5 ± 1.5%, 25.9 ± 2.1%, and 11.9 ± 2.0% of the basal volume, respectively. The dependence of the gallbladder emptying on the dose of cerulein was described by the equation of linear regressiony –21.33 [ln(dose + 1)] + 95.81 (r=–0.963,P<0.001). Accordingly, the cerulein dose required to evoke a 50% reduction of the gallbladder volume amounted to 7.6 pmol/kg/hr (95% confidence interval: 6.8–8.6 pmol/kg/hr). A plateau at the level of about 44% of the basal gallbladder volume characterized the time-course of the gallbladder emptying between 20 and 60 min of the infusion at a constant rate of 7.4 pmol/kg/hr. On the other hand, the 1-hr infusion of 22.2 pmol/kg/hr evoked a continuous decrease in the gallbladder volume with a nadir of 10.2 ± 0.7% achieved at 60 min. Refilling of the gallbladder, contracted after a 1-hr infusion of cerulein, was complete within 30 and 60 min after the end of infusion for rates of 7.4 pmol/kg/hr and 22.2 pmol/kg/hr, respectively. The time course of the gallbladder filling after cessation of 1-hr infusion of cerulein at 7.4 pmol/kg/hr was described by the equation of linear regression of relative gallbladder volumes vs time:y=1.732x + 48.61 (r=0.739,P < 0.001). Refilling of the gallbladder was faster during the first 30 min (y=2.191x+7.13,r=0.885,P<0.001) and slower between 30 and 60 min (y=1.218x + 74.97,r=0.533,P < 0.001) after the end of a 1-hr infusion of cerulein at a rate of 22.2 pmol/kg/hr.     

Gallbladder dynamics in chronic pancreatitis

Gallbladder dynamics, cholecystokinin (CCK), and pancreatic polypeptide (PP) release were studied in 14 patients with chronic pancreatitis (CP) (2 females, 12 males; age range 24–56 years) and 12 control subjects (4 females, 8 males, 21–50 years). On day 1, gallbladder contractility was investigated after ceruletide intravenous infusion (2.5 ng/kg/min for 10 min). On day 2, a mixed standard test meal (1450 kJ) was administered orally. Gallbladder volume was assessed at three time intervals before (–30, –15, 0 min) and at 5, 10, 20, 30, 40, 50, 60, 80, 100 and 120 min after stimulation by means of ultrasonography. CCK and PP plasma levels were determined at each time interval.Exocrine pancreatic function was assessed using the pancreolauryl serum test (PLT). Six patients with CP had severe exocrine pancreatic insufficiency (EPI) (PLT<1.8 g/ml) with steatorrhea, eight patients had mild-moderate EPI. Fasting gallbladder volume was increased in CP (32.3±3.1 cm³) as compared to controls (20.5±1.2 cm³) (P<0.01). Peak gallbladder contraction (percent of initial volume) in CP ranged from 5 to 55% (controls: 8–46%) following ceruletide and from 17 to 86% (controls: 27–80%) following the test meal (NS). There was no correlation between the degree of EPI according to PLT and peak gallbladder contraction. Gallbladder emptying in CP patients was not different from controls, although the postprandial CCK response was significantly impaired (P<0.01). Postprandial PP response in CP was correlated with the PLT result (r=0.78;P<0.01) but not with gallbladder emptying or refilling time. We conclude that gallbladder emptying and refilling following the oral administration of a test meal or the stimulation with a pharmacological dose of ceruletide is normal in patients with chronic pancreatitis. Postprandial gallbladder emptying is not influenced by the degree of exocrine pancreatic insufficiency.     

The effect of acute oral erythromycin on gallbladder motility and on upper gastrointestinal symptoms in gastrectomized patients with and without gallstones: a randomized, placebo-controlled ultrasonographic study

OBJECTIVE: Gastrectomy might be a risk factor for cholelithiasis and gallbladder stasis might play a major role. We studied fasting and postprandial gallbladder motility with 600 mg oral erythromycin or placebo in gastrectomized patients (with and without gallstones) and controls. METHODS: Seventeen patients operated on for gastric cancer (subtotal gastrectomy: n = 10, total gastrectomy: n = 7) were compared with 20 sex- and body-size matched healthy controls. Subjects randomly received erythromycin or placebo 30 min before the ingestion of a standard 200 ml liquid test meal. Gallbladder volume was estimated by ultrasonography until 120 min after test meal. A visual analog scale monitored GI perception of appetite, satiety, nausea, abdominal fullness and epigastric pain. RESULTS: Gastrectomized patients had increased fasting gallbladder volume (35.9 +/- 3.4 ml versus 21.0 +/- 1.4 ml, p = 0.0005) with faster postmeal emptying (T/2 14.8 +/- 1.1 min versus 23.5 +/- 1.5 min, p = 0.00019) than controls. Six patients developed small and asymptomatic gallstones, which did not influence gallbladder motility. In these patients, fasting gallbladder volume increased with time after surgery (r = +0.82, p = 0.047). Perception of satiety, abdominal fullness, and epigastric pain after ingestion of the test meal were all significantly greater in patients than in controls. Erythromycin significantly enhanced gallbladder emptying during fasting (p = 0.001) and postprandially in both patients and controls (0.002 < p < 0.017) and significantly reduced postmeal satiety and epigastric discomfort in gastrectomized patients. CONCLUSIONS: Increased fasting volume might be a form of stasis, predisposing patients to gallstone formation. Erythromycin improves fasting and postprandial gallbladder emptying and decreases upper GI symptoms in gastrectomized patients.     

Gallbladder function and gastric liquid emptying in achalasia

Because of evidence that the abnormalities in achalasia are not restricted to the distal esophagus, we investigated gallbladder function by cholescintigraphy in the steady state and in response to CCK and the scintigraphic gastric emptying of a liquid caloric meal in 10 individuals with achalasia and 10 normal controls. No abnormalities were found during the filling phase of the gallbladder but seven of the 10 patients showed a 50% reduction in the ejection fraction (39.4%±30.4 vs 80.3±8.3 of controls, mean±sd,P=0.007) and a slower than normal ejection phase (9.1%/min±6.6 vs 18.1±4.5,P=0.02. In eight of the 10 patients, gastric liquid emptying was accelerated with a T1/2 of 41.5 min±15.4 vs 74.7 min±11.5 in the controls (P=0.007). It is concluded that in some achalasia patients extraesophageal functional abnormalities of the gastrointestinal tract may be found. Whether these findings are promoted by degenerative changes of extraesophageal nerve fibers as well as their clinical significance require further investigations.This paper was presented as abstract at the American Gastroenterological Association Meeting, San Antonio, Texas, in May 1990.     

Effect of Endoscopic Sphincterotomy on Gallbladder Motility

In experimental animals, sphincterotomyfacilitates passage of solids from the gallbladder andinhibits gallstone formation apparently by improvementin gallbladder emptying. In humans, however, gallbladder emptying has not been studied followingendoscopic sphincterotomy (ES) in patients withgallstones. We therefore prospectively studied restingand cerulinstimulated gallbladder volumes by real timeultrasonography in 15 patients of choledocholithiasis withgallbladder in situ (eight with and seven withoutgallbladder calculi) before and after (after bile ductclearance) ES. ES significantly lowered restinggallbladder volume (21.2 ± 10.6 vs 11.1 ±5.0; P < 0.0001) and cerulin-stimulated residualgallbladder volume (10.8 ± 5.6 vs 4.4 ±2.1; P < 0.0001). ES also significantly increased thegallbladder ejection fraction (47.3 ± 12.1% vs 58.8 ± 11.1%; P < 0.0001). Therate constant for gallbladder emptying after cerulininfusion also increased significantly after ES(–0.022/min vs –0.031/ min; P < 0.0001).Significant improvement in gallbladder motility was observed in both groups ofpatients with and without gallbladder calculi. ESsignificantly improves gallbladder motility inhumans.     

Inhibitory reflexive effect of rectal distension on postprandial gastric myoelectrical activity

The aim of the study was to determine the effects of low-volume rectal distension on gastric myoelectrical activity. The study was performed in 14 healthy volunteers in 2 randomized sessions. In the control session, a small balloon was inserted into the rectum 10 cm beyond the anal verge and inflated with 20 ml of air. Gastric myoelectrical activity was recorded for 30 minutes in the fasting state and 30 minutes after a meal; and then the balloon was deflated and removed, and another 30-min recording was followed. The study session was the same except that after the 30-min baseline recording the balloon was inflated to reach a volume with which the subject felt an urgency for defecation. Spectral analyses were performed to compute the dominant frequency, power, and regularity (2–4 cycles/minutes, cpm) of the gastric slow waves and the percentage of gastric dysrhythmia. Results: 1). In comparison with our previously published data, the placement of the rectal balloon with a volume of 20 ml air did not affect the regularity of the slow waves (84.2 ± 3.6% in fasting, 85.3 ± 4.3% in fed); In comparison with the control session, the rectal distension inducing an urgency for defecation (average volume of air: 72.5 ml) significantly reduced the regularity of gastric slow waves in the fed state (72.0 ± 5.7%, P < 0.03 vs baseline; P < 0.02, vs control session) but not in the fasting state (80.1 ± 4.5%, P = 0.1). This postprandial change was attributed to a significant increase in bradygastria (3.1 ± 1.0% vs 7.9 ± 2.6%, P < 0.04) and a marginal increase in tachygastria (7.4 ± 2.5% vs 15.8 ± 4.3%, P = 0.06). The normal postprandial increases in the dominant frequency and power of the gastric slow wave were abolished in both sessions. conclusions, rectal distension evoking an urgency for defecation impairs postprandial gastric slow waves with an increase in the percentage of both bradygastria and tachygastria.     

Gallbladder emptying in patients with primary sclerosing cholangitis

AIM： To assess gallbladder emptying and its association with cholecystitis and abdominal pain in patients with primary sclerosing cholangitis （PSC）. METHODS： Twenty patients with PSC and ten healthy subjects were investigated. Gallbladder fasting volume, ejection fraction and residual volume after ingestion of a test meal were compared in patients with PSC and healthy controls using magnetic resonance imaging. Symptoms, thickness and contrast enhancement of the gallbladder wall and the presence of cystic duct strictures were also assessed. RESULTS： Median fasting gallbladder volume in patients with PSC [67 （19-348） mL] was twice that in healthy controls [32 （16-55） mL] （P 〈 0.05）. The median postprandial gallbladder volume in patients with PSC was significantly larger than that in healthy controls （P 〈 0.05）. There was no difference in ejection fraction, gallbladder emptying volume or mean thickness of the gallbladder wall between PSC patients and controls. Contrast enhancement of the gallbladder wall in PSC patients was higher than that in controls; （69% ± 32%） and （42% ± 21%） （P 〈 0.05）. No significant association was found between the gallbladder volumes and occurrence of abdominal pain in patients and controls.CONCLUSION： Patients with PSC have increased fasting gallbladder volume. Gallbladder Mucosal dysfunction secondary to chronic cholecystitis, may be a possible mechanism for increased gallbladder.     

Correlation between gall bladder fasting volume and postprandial emptying in patients with gall stones and healthy controls.

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.     

内镜乳头括约肌切开对胆囊排空功能的影响

目的观察乳头括约肌切开术(EST)对胆囊排空功能的影响。方法以超声测定38例患 者行EST前1d，术后2周、1月、3月的空腹胆囊体积；并于脂餐后20～120min每隔20min检测餐后胆囊体积，以不同时间的最小值计算出胆囊排空率。结果EST术后空腹胆囊体积及脂餐后胆囊体积较术前明显缩小，1月后趋于稳定，在术后3月空腹胆囊体积由术前(31.4±10.6)ml下降为(17.2±8.7)ml，差异有非常显著性(P＜0.01)；脂餐后胆囊体积由(18.2±5.6)ml下降为(7.1±2.5)ml，差异有非常 显著性(P＜0.01)；胆囊排空率由(4l.9±13.4)％上升为(59.9±11.7)％，差异有非常显著性(P＜0.01)。结论EST后胆囊排空功能增强。