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PubMed1987

[Ultrasonic study of gallbladder motility during exclusive continuous enteral feeding].

Total parenteral nutrition may be responsible for gallbladder sludge and lithiasis which might possibly be related to gallbladder bile stasis. Gallbladder motility has not yet been studied during constant-rate enteral nutrition. We performed serial ultrasonographic studies of gallbladder volume and contents in ten patients receiving constant-rate enteral nutrition during 35 +/- 17 days. Each patient had two weekly examinations at 9 AM and 2 PM on the same day. None of the patients developed gallbladder sludge or lithiasis. The gallbladder was frequently seen to be contracted. Mean gallbladder volume during constant-rate enteral nutrition was not significantly different from mean gallbladder volume after Bladex. Individual gallbladder volume changed significantly from one measurement to another. This study showed that gallbladder motility is preserved during constant-rate enteral nutrition. The persistence of gallbladder contractions may prevent the development of biliary sludge ad lithiasis.

Adolescent↗

PubMed1984

[A clinical study on cefotiam with special reference to excretion in bile and concentration in gallbladder tissue].

Following 1 hour intravenous drip infusion of 1.0 g of cefotiam (CTM), 38 patients with cholelithiasis were operated at scheduled intervals. The CTM concentrations in serum, common duct bile, gallbladder bile and gallbladder tissue were measured. The mean level of CTM concentration in serum showed a peak of 53.1 micrograms/ml at 1 hour, and decreased in the level of 1.0 microgram/ml at 5 hours after administration. CTM concentrations in common duct bile revealed a mean level of 162 micrograms/ml at 1 hour and similarly high concentrations from 1 to 5 times of the peak level in serum were maintained for 3.5 hours. In patients with impaired liver function, the levels of CTM concentration were lower than those without them. CTM concentrations in gallbladder bile showed a high value at 2-3.5 hours after administration . In many cases the levels were relatively lower than those in common duct bile, particularly ion patients with cystic duct obstruction and/or with marked chronic cholecystitis. As for gallbladder tissue levels, CTM concentrations showed low levels less than 50 micrograms/g in patients with pathological changes of gallbladder, as well as in gallbladder bile. While, favorable concentrations of 50-100 micrograms/g were obtained in patients without them. There was a positive correlation between CTM concentrations in common duct bile and gallbladder bile, and also between the concentrations in gallbladder bile and those in gallbladder tissue in patients without cystic duct obstruction or marked chronic cholecystitis. Then, in the situation, CTM transfer into gallbladder bile or gallbladder tissue might be mainly dependent on biliary excretion of CTM.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Enhancement of gallbladder emptying in gallstone patients after oral cholestyramine.

OBJECTIVE: To evaluate whether a low dose of oral cholestyramine improves gallbladder emptying in gallstone patients. METHODS: Gallbladder volumes were assessed by sonography in 36 patients with cholesterol gallstones and 18 healthy controls. On three different days subjects ingested: 1) test meal alone, 2) test meal plus cholestyramine (4 g), and 3) cholestyramine alone (4 g). RESULTS: Fasting gallbladder volume (mean +/- SE, 25.9 +/- 1.8 ml and 19.2 +/- 1.3 ml for patients and controls, respectively, p < 0.05) and postprandial gallbladder residual volume (48.7 +/- 3.9% and 21.6 +/- 2.8% of fasting volume in patients and controls, respectively, p < 0.001) were larger in patients than controls, indicating impaired gallbladder emptying. Gallstone patients were divided into 19 "contractors" and 17 "hypocontractors" (residual gallbladder volume smaller or greater than mean +/- 2 SD of controls). Compared with the test meal alone, the addition of cholestyramine induced a further decrease of residual volume in contractors (from 30.4 +/- 2.1% to 19.8 +/- 1.9%, p < 0.001), hypocontractors (from 69.3 +/- 3.9% to 56.7 +/- 7.4%, p < 0.05), and controls (from 21.6 +/- 2.8% to 5.0 +/- 1.0%, p < 0.0004). Two hours after test meal plus cholestyramine gallbladder volume was still markedly reduced in both patients and controls. Fasting gallbladder volume 24 h after test meal plus cholestyramine was decreased in patients and in controls. The ingestion of cholestyramine alone initiated gallbladder evacuation comparable to that of test meal in both contractors and hypocontractors. CONCLUSIONS: A low dose of cholestyramine in combination with test meal induces a considerable decrement of gallbladder volume compared with test meal alone in gallstone patients. Cholestyramine alone causes a decrease of gallbladder volume which is comparable to that observed in response to test meal alone.

Administration, Oral↗

PubMed1993

[Effect of a low-fat diet on the fasting volume and postprandial emptying of the gallbladder].

Little is known of the effects of meal composition on gallbladder emptying and cholecystokinin (CCK) release in man. Gallbladder volumes (measured by means of real time ultrasonography) and plasma CCK levels (determined by radioimmunoassay) were studied in 5 normal subjects, before and after a normal solid-liquid meal, and before and after a low-fat, low-protein, solid-liquid meal after 3 days regimen with low-fat, low-protein meal. Low-fat, low-protein regimen significantly increased gallbladder fasting volume and significantly decreased fasting plasma CCK levels. This suggests that CCK secretion regulates fasting gallbladder volume and that basal CCK secretion depends on diet composition. After a normal meal, gallbladder emptying was biphasic with a 44% volume decrease within the first 15 min followed by slower emptying during the next 60 min with a final volume reaching less than 15% of the fasting volume. After a hypolipidic, hypoproteic meal, the initial 15 min emptying (42%) was the same as after control meals but no further decrease of gallbladder volume was observed. This study shows that the initial phase of post prandial gallbladder contraction is not dependent on meal composition which affects late gallbladder emptying only. We conclude that a low-fat, low-protein diet, increasing gallbladder fasting volume and decreasing gallbladder emptying, may favor gallbladder stasis and therefore increase the risk of gallstone formation.

Cholecystokinin↗

PubMed1996

Gallbladder dyskinesia in acalculous biliary colic.

AIMS: To test the hypotheses that: 1) postprandial gallbladder emptying might be abnormal in patients with acalculous biliary colic; and 2) that hymecromone, a drug that increases bile flow and relaxes biliary muscle might improve symptoms. METHODS: Twenty-four women were studied. Twelve patients presented recurrent biliary type of pain in the absence of gallstones, and persistence of contrast in the gallbladder, 24 hours after an oral cholecystogram, suggesting cholesterolosis. Twelve healthy volunteers used as controls had no symptoms and the gallbladder was not visible the day after an oral cholecystogram. Gallbladder emptying induced by an oral meal was studied with ultrasound in both groups before and after the administration of hymecromone. RESULTS: Gallbladder volumes were similar in both groups (23 +/- 10 ml vs. 31 +/- 11 ml; NS). Gallbladder emptying in the control group was simple exponential (R2 = 0.948 +/- 0.059) with a rate of 32 +/- 16 minutes. Gallbladder emptying was bimodal in patients. Gallbladder volume increased to 120% in the first 10 minutes, to empty exponentially thereafter (R2 = 0.964 +/- 0.040. Rate: 29 +/- 22 minutes). This resulted in a marked reduction in gallbladder volume emptied at 40 minutes when compared to controls (30% +/- 27% vs. 54% +/- 14%; p = 0.012). Pretreatment of controls with hymecromone induced an emptying pattern similar to that of patients. In patients, emptying after hymecromone did not change but symptoms were improved. CONCLUSIONS: An abnormal emptying pattern of the gallbladder was identified in patients with acalculous biliary colic, and hymecromone was partly effective to reduce pain, despite a minor effect on gallbladder emptying pattern.

Biliary Tract Diseases↗

PubMed1997

Retrospective analysis of 70 operations for gallbladder carcinoma.

BACKGROUND: The clinical course of patients with carcinoma of the gallbladder depends on the depth of tumour invasion. This study was conducted to clarify the prognostic factors affecting survival and appropriate surgical strategy based on depth of invasion of gallbladder carcinoma according to the pathological tumour node metastasis (pTNM) classification. METHODS: A total of 70 patients who underwent surgical resection were reviewed retrospectively with regard to the type of operation, histopathological findings of the resected gallbladder carcinoma and clinical follow-up after operation. RESULTS: Twelve patients with pT1 gallbladder carcinoma fared favourably following cholecystectomy or extended cholecystectomy. In 13 of 26 patients with pT2 gallbladder carcinoma, lymph node metastasis was evident: pN1 in eight and pN2 in five. The 3-year survival rate of patients with pT2 gallbladder carcinoma was 28 per cent after cholecystectomy, 91 per cent after extended cholecystectomy and 67 per cent after hepatectomy. In 21 of 28 patients with pT3 or pT4 gallbladder carcinoma, surgical margins were affected by malignant cells. The 1-year survival rate of patients with pT3 or pT4 gallbladder carcinoma was 24 per cent, even after hepatectomy. Significant prognostic factors were age, macroscopic type, histological grade, depth of invasion, lymph node metastasis, pathological stage, lymphatic invasion, venous invasion, perineural invasion and involved surgical margins. CONCLUSION: Cholecystectomy was adequate for pT1 gallbladder carcinoma. Extended cholecystectomy or hepatectomy with extrahepatic bile duct resection and lymph node dissection (pN1 and pN2) were justified for pT2 gallbladder carcinoma. The survival of patients with more advanced gallbladder carcinoma remains dismal.

Adult↗

PubMed1997

The role of cholecystokinin and the cholinergic system in intravenous amino acid-induced gallbladder emptying.

BACKGROUND: Recent studies have demonstrated that separate intravenous infusion of amino acids (IVAA) at high doses induces gallbladder emptying. However, little is known about the mechanisms mediating IVAA-induced gallbladder contraction. OBJECTIVE AND METHODS: To investigate whether the effect of IVAA on gallbladder motility is mediated by the cholinergic system and/or cholecystokinin (CCK), the major hormonal stimulus for gallbladder contraction. Six healthy male volunteers were studied in random order on five occasions using: (a) IVAA, (b) loxiglumide (CR 1505, a selective CCK-A receptor antagonist), (c) IVAA plus loxiglumide, (d) atropine and (e) IVAA plus atropine. Gallbladder volumes (ultrasonography) and plasma CCK levels (radioimmunoassay) were determined every 15 min for 60 min before and for 120 min during intravenous infusion of amino acids (Vamin 18EF; 250 mg protein/kg/h) and/or loxiglumide (10 mg/kg/h) and/or atropine (0.005 mg/kg/h). RESULTS: IVAA significantly (P < 0.05) reduced gallbladder volume from 32 +/- 5 ml to 17 +/- 2 ml but induced only a small and transient increase in plasma CCK levels. Loxiglumide given alone significantly (P < 0.05) increased fasting gallbladder volume to 190% of the basal value. IVAA-induced gallbladder emptying was completely abolished by loxiglumide. Maximal gallbladder relaxation during IVAA plus loxiglumide was not significantly different compared to loxiglumide given alone. Concomitant administration of atropine also significantly (P < 0.05) inhibited IVAA-induced gallbladder emptying. CONCLUSION: In healthy volunteers intravenous infusion of high doses of amino acids results in a significant gallbladder contraction, which is inhibited by CCK-A receptor blockade and by atropine.

Adult↗

PubMedDate not supplied

Three-dimensional sonographic evaluation of gallbladder contractility: comparison with cholescintigraphy.

PURPOSE: To compare three-dimensional sonography (3D US) with quantitative cholescintigraphy for assessing gallbladder contractility. METHODS: Gallbladder radioactivity was assessed in 35 patients with suspected gallbladder disease using a gamma camera 5, 30, 60, and 90 minutes after technetium 99m (Tc-99m) DISIDA injection and 30 and 60 minutes after ingestion of a high-fat meal. Immediate gallbladder images were obtained via 3D US. Gallbladder radioactivity at 120 minutes after injection of Tc-99m DISIDA was defined as 100%, and gallbladder contractility was calculated. Gallbladder volume on 3D US was calculated using a dedicated software. Pearson correlation analysis and simple linear regression analysis were used. RESULTS: The mean gallbladder volume on 3D US was 25.3 ml after fasting and 6.6 ml after a high-fat meal. The mean gallbladder contractility index was 77.7% on cholescintigraphy (range, 18-99) and 73.4 on 3D US (range, 16.7-97.3). A linear correlation between cholescintigraphy and 3D US contractility indices was observed. The r value on Pearson analysis was 0.92 and R(2) of the coefficient of determination was 0.85. The difference in measured contractility between the 2 methods ranged from +21.5% to -15.0% (mean +/- SD, 4.4 +/- 8.7%). CONCLUSIONS: 3D US is a reliable and easy method for clinical measurement of the volume of the gallbladder and its contractility.

Gallbladder↗

PubMed2004

Chemical mediators of gallbladder dysmotility.

In order to accomplish its contribution to the digestive process, the gallbladder must contract appropriately during its emptying phases and it must be able to relax adequately for filling to occur. A variety of neuro-hormonal inputs to gallbladder smooth muscle coordinate the gallbladder emptying process with other events occurring in the bowel. Gallbladder dysmotility can disrupt the normal flow of bile to the small bowel, resulting in digestive dysfunction. In addition to this, alterations in gallbladder motility may play a role in pathological conditions, such as cholesterol gallstone formation and cholecystitis. It is still not entirely clear whether impaired gallbladder emptying is a cause or consequence of cholesterol gallstones, but recent experimental evidences demonstrate that cholesterol can directly affect the plasma membrane of gallbladder smooth muscle cells to cause impaired contraction. In addition, gallbladder emptying is impaired in acute gallbladder inflammation, probably as the result of the deleterious neural and muscular actions of inflammatory mediators such as reactive oxygen species, prostaglandins and histamine. It should also be noted that opiate treatments in critically ill patients can reduce gallbladder motility by inhibiting neurotransmitter release, and may contribute to the onset of acalculous cholecystitis, which is associated with significant morbidity in these patients.

Acalculous Cholecystitis↗

PubMed1982

Strong acoustical shadowing from the gallbladder bed: ultrasonic-pathologic correlation.

We reviewed a series of 25 patients whose cholecystosonograms showed ultrasonic nonvisualization of the gallbladder, high-amplitude echoes in the region of the gallbladder bed, and strong acoustical shadowing. These 3 findings have previously been thought to be a reliable indication of a small contracted gallbladder filled with stones. In our series, all 25 such patients did not have gallstones, but the size and number of the calculi were highly variable. Only a small minority of our patients had a contracted gallbladder in most, the volume of the gallbladder was either normal or greater than normal. Ultrasonic nonvisualization of the gallbladder accompanied by acoustical shadowing was not a reliable indicator of gallbladder wall thickness in our series. Of 25 patients, 20 had either a normal gallbladder wall or only slight thickening. When we reviewed our images to determine how many fit the "WES" criteria thought to be a specific manifestation of a contracted gallbladder filled with stones, we found that 14 of 25 individuals clearly showed this group of ultrasonic findings. We could not, however, correlate the presence or absence of the 'WES' triad with the number and size of stones, the gallbladder volume, or thickness of the gallbladder wall.

Cholelithiasis↗

PubMed1986

Transport of fluid and biliary lipids in the canine gallbladder in experimental cholecystitis.

In acute cholecystitis the cystic duct is usually obstructed by a gallstone and the gallbladder is often tensely distended with clear fluid. Because these findings suggest that fluid absorption in the gallbladder may be reversed in cholecystitis, we examined the effect of inflammation on the gallbladder mucosal function in dogs. In 20 dogs cholecystitis was induced by ligating the cystic duct and allowing inflammation to develop from bile stasis and the presence of a chronic indwelling cannula in the gallbladder. Every morning an aliquot of normal hepatic bile was infused into the gallbladder through a cannula in the gallbladder fundus. After either 4 or 24 hr the gallbladder contents were aspirated, the volume was measured, and the concentrations of bile acids, cholesterol, phospholipids, and protein were determined. Changes in volume were checked using [14C]PEG as a nonabsorbable tracer. A net absorption of fluid, bile acids, cholesterol, and phospholipids occurred during the first 24 to 48 hr after ligation of the cystic duct. Thereafter, fluid, cholesterol, and protein were secreted into the lumen, but absorption of bile acids continued. The lithogenic index of bile placed in the inflamed gallbladder was always greater when the bile was removed 24 hr later. The rate of fluid secretion into the lumen of the inflamed gallbladder increased after a meal and decreased after indomethacin. These findings demonstrate that inflammation can stimulate the gallbladder mucosa to secrete fluid, a process that may be important in the pathophysiology of acute cholecystitis in man. Since inflammation also resulted in an increased cholesterol saturation of gallbladder bile, cholecystitis per se may contribute to the formation of cholesterol gallstones.

Animals↗

PubMed1987

The role of prostaglandins E and F in acalculous gallbladder disease.

Prostaglandins have been postulated to be involved in the formation of gallstones and the pain and inflammation of calculous gallbladder disease. This report evaluated prostaglandin E and F levels in patients with acalculous gallbladder disease. Control gallbladders were obtained from patients undergoing cholecystectomy during insertion of hepatic artery catheters for regional, hepatic chemotherapy. Patients without gallstones and with long-standing post-prandial biliary colic with abnormal cholecystokinin administration underwent cholecystectomy for chronic acalculous cholecystitis. A third group of patients underwent cholecystectomy for acute acalculous cholecystitis. Gallbladder mucosa and muscle were separated, and prostaglandin E and F concentrations in mucosal and muscle or mucosa were identified in gallbladders from patients with chronic acalculous cholecystitis compared to gallbladders from patients without biliary tract symptoms. In gallbladders from patients with acute acalculous cholecystitis a seven-fold increase in PGE production by muscle tissue and mucosal cells was found. The more histologically inflamed gallbladders had higher mucosal and muscle prostaglandin E concentrations than were found in less inflamed gallbladders. Prostaglandin F levels were not significantly changed or were decreased, resulting in a significant increase in the ratio of PGE/PGF in acutely diseased gallbladders when compared to normal gallbladders. Prostaglandin E may be a manipulatable intermediary in the sequence of events that results in the development of acute acalculous cholecystitis.

Acute Disease↗

PubMed1999

Laparoscopic cholecystectomy and unsuspected gallbladder carcinoma.

Gallbladder cancer is a relatively uncommon malignancy in the United States. Its presentation is similar to that of lithic disease of the gallbladder. Laparoscopic cholecystectomy has become the method of choice for removing the gallbladder in most benign conditions. Occasionally, unsuspected gallbladder carcinoma is encountered in association with laparoscopic cholecystectomy. Overall, gallbladder cancer portends a poor prognosis. However, in select cases, a favorable outcome can be expected and the less favorable predicted expected outcome can be improved. Management of patients with gallbladder cancer in different situations is discussed: gallbladder cancer noted postoperatively on final pathology, gallbladder cancer noted after removal of the gallbladder and opening of the specimen at the time of surgery, difficulty encountered at the time of dissection and resultant suspicion of gallbladder cancer, and diagnosis of extensive disease at initial placement of the laparoscope. The technique of extended cholecystectomy is outlined.

Carcinoma↗

PubMed1992

Gallbladder hypokinesia and normal gastric emptying of liquids in patients with dyspeptic symptoms. A double-blind placebo-controlled clinical trial with cisapride.

Gastric and gallbladder emptying after a standard liquid meal were studied in 65 patients with early satiety, bloating, pain at the right hypochondrium or the epigastrium, nausea, and occasionally vomiting. Fifty normal subjects were studied as a control group. Gastric and gallbladder emptying were evaluated by means of real-time ultrasonography (RUS). Serial RUS scans were made after a 12-hr fast and every 15 min after a standard meal for 2 hr. Patients were considered to have delayed gastric emptying or hypokinetic gallbladder when gastric diameters and gallbladder volume evaluated 45 min after meal were 2 SD above the corresponding mean values of the normal subject group. Fifteen patients (23%) were found with delayed gastric emptying and 20 (30.7%) a reduced gallbladder emptying. None of our patients showed delayed gastric emptying and hypokinetic gallbladder simultaneously. The 20 patients with reduced gallbladder emptying were included in a double-blind randomized, placebo controlled, change-over study with cisapride (10 mg three times a day) for 30 days. Cisapride treatment reversed the gallbladder hypomotility within the normal range while placebo did not change the response to meal. Symptom score improved significantly after cisapride and placebo. It is concluded that in dyspeptic patients with reduced gallbladder response to a meal cisapride may be of help in improving the kinetic abnormality. Dyspeptic symptoms, however, do not seem to be corrected with the described gallbladder motor abnormality.

Adult↗

PubMed1997

Simultaneous assessment of gallbladder emptying in the dog by real-time ultrasonography and strain gauge.

Patterns of meal- and cerulein-induced gallbladder emptying (GBE) were compared in four dogs equipped with a force transducer implanted onto the body of the gallbladder, and in four unoperated animals. GBE was examined by real-time ultrasonography in conscious dogs. In two dogs the ultrasonographic measurement of GBE was performed simultaneously with the registration of the strain exerted on the force transducer fixed on the gallbladder body. Implantation of the force transducer onto the gallbladder impaired neither postprandial nor cerulein-induced GBE. The contractile response of the gallbladder exhibited a non-linear relationship to the gallbladder volume. The reduction of gallbladder volume to 50% of its basal value was accompanied by an increase in strain amounting to about 16% of the maximum response, whereas a pronounced augmentation of the strain was observed with gallbladder volume ranging between 30% and 10% of the basal value. On the other hand, the contractile response of the gallbladder registered by means of a force transducer was linearly related to the angle alpha contained between two radii passing from the gallbladder center towards the edges of the strain gauge: y = 0.852 alpha-30.97 (r = 0.959, P < 0.001) in the case of i.v. cerulein infusion at stepwisely increasing doses (0.7-2.2-7.4-22.2-66.5 pmol.kg-1 h-1), and y = 0.640 alpha-17.40 (r = 0.869, P < 0.001) for a 1-h constant-rate 22.2 pmol.kg-1 h-1 cerulein infusion.

Animals↗

PubMed2003

[Dynamic ultrasonography in the diagnosis of gallbladder dysfunction: reliability of a simple method with easy clinical application].

AIMS: Although the results of dynamic ultrasonography (DUS) are similar to those of dynamic cholescintigraphy (DCS) in the study of gallbladder function, the methodology required for this technique is laborious and sometimes complex. The aim of this study was to investigate the reliability of a simple method of DUS to evaluate gallbladder function using DCS as a reference. PATIENTS AND METHODS: Gallbladder function was studied using DUS and DCS in 80 consecutive patients with clinical findings compatible with gallbladder dysfunction. For DUS the ellipsoid method was used with measurement of three gallbladder diameters (transversal, longitudinal and anteroposterior) in basal conditions and after applying a cholecystokinetic stimulus (meal test); gallbladder emptying of less than 50% was considered abnormal. In DCS intravenous cholecystokinin (CCK) (0.40 IDU/kg in 20 minutes) was used as stimulus and an ejection fraction < or = 40% was considered abnormal. RESULTS: In 15 patients (19%; 95% CI, 11-29%) abnormal gallbladder response was found using DUS. The ejection fraction in the entire group of patients studied was 48 26.2%. Ejection fraction was abnormal in 41 patients (51%; 95% IC, 40-63%) with a value of 25 8.5% and was normal in 39 patients (49%; 95% IC, 40-63%) with a value of 71.5 14.5%. The correlation coefficient between the values of gallbladder emptying calculated with DUS and the ejection fraction obtained with DCS was 0.199 (p = 0.079). When patients were divided according to gallbladder emptying measured by DUS and the ejection fraction obtained with DCS the concordance was very low (k = 0.065; EE = 0.085). CONCLUSIONS: DUS performed using a simple technique lacks diagnostic value in gallbladder dysfunction when DCS is taken as a reference test

Adult↗

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↗

PubMed2004

Effects of growth hormone deficiency and recombinant growth hormone therapy on postprandial gallbladder motility and cholecystokinin release.

In addition to cholecystokinin, other hormones have been suggested to be involved in regulation of postprandial gallbladder contraction. We aimed to evaluate effects of growth hormone (GH) on gallbladder contractility and cholecystokinin release. Gallbladder and gastric emptying (by ultrasound) and cholecystokinin release were determined before and after 6 months of recombinant human GH (rhGH) therapy in 12 patients with GH deficiency, after either a mixed (n = 5) or a liquid (n = 7) meal. Basal postprandial gallbladder contraction was severely impaired (19 +/- 2 and 26 +/- 3% of fasting volume after mixed and liquid meal, respectively). Histology and cholecystokinin sulfation patterns in duodenal biopsies from two patients were normal. After 6 months of rhGH therapy, fasting gallbladder volumes increased (from 20.8 +/- 0.9 to 25.9 +/- 1.1 mL, P < 0.05) and postprandial gallbladder emptying was restored (70 +/- 6 and 70 +/- 7% of fasting volume after mixed and liquid meal, respectively), without change of gastric emptying. Cholecystokinin secretion after a mixed meal and gallbladder sensitivity to cholecystokinin were significantly enhanced during rhGH replacement compared to the basal state. Postprandial cholecystokinin release, gallbladder responsiveness to cholecystokinin, and gallbladder emptying are severely impaired in the absence of GH. Reversibility during GH suppletion suggests its involvement in regulation of gallbladder contractility.

Adolescent↗