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PubMed1980

Computed tomography of gallbladder carcinoma.

Twenty-seven gallbladder carcinomas were examined by computed tomography (CT). All patients had abnormal CT findings, suggesting a gallbladder lesion in 26. Based on the major CT findings, gallbladder cancer was classified as "massive," "thickened wall," or "intraluminal." Twenty cases were diagnosed correctly as cancer: on retrospect, definite findings of gallbladder cancer were observed in 24 and equivocal or misleading signs in 3. Some cases of chronic cholecystitis and liver tumor were difficult to differentiate from gallbladder cancer. Direct hepatic extension was easily seen, but lymph-node metastases and bile-duct extension were difficult to distinguish.

Adenocarcinoma↗

PubMed1982

Percutaneous ultrasound-guided puncture of the gallbladder (PUPG).

Percutaneous ultrasound-guided puncture of the gallbladder (PUPG) is a new method for antegrade study of the gallbladder and the common bile duct. All procedures were scheduled immediately prior to planned surgery. Under ultrasound guidance, a 22-gauge sheathed needle was placed into the gallbladder lumen, and dilute (25% to 30%) diatrizoate meglumine (Hypaque) was injected. Indications in five patients included: evaluation of the common bile duct for calculi and/or obstruction, specifically in one patient who had hypersensitivity to intravenous contrast material; aspiration of bile for gram stain, crystal analysis, and cytology; evaluation of the gallbladder lumen for intraluminal masses; and to establish the anatomic site of an occult abscess. A small bile leak occurred in one patient who had no obstruction, and a more significant leak occurred in a patient who had obstructive jaundice and ampullary carcinoma. PUPG obviated the need for surgical intervention in three patients. Although the method has limited indications, we feel that it has great diagnostic potential in conditions related to the gallbladder and biliary ducts.

Adult↗

PubMed1985

Contracted gallbladder: a finding in hepatic dysfunction.

A review of ultrasound (US) examinations of 35 patients with acute hepatitis revealed 6 patients who had contracted gallbladders despite adequate fasting prior to the examination. After the acute phase of their hepatitis had resolved, four patients had normal gallbladders on US. One patient who did not recover was found at autopsy to have a normal but contracted gallbladder. It is suggested that acute hepatic dysfunction may decrease the flow of bile into the gallbladder, resulting in a gallbladder that is transiently contracted or is not visualized on US.

Acute Disease↗

PubMed1985

Differentiation of benign from malignant ascites by sonographic evaluation of gallbladder wall.

The gallbladders of 65 patients with ascites were examined on ultrasonograms. In 37 patients, the thickness of the gallbladder wall was less than or equal to 3 mm and was considered normal or "single." In 28 patients, the gallbladder wall thickness was greater than or equal to 4 mm, with a central echo-free zone giving the appearance of a double wall. Of the 37 patients with single-walled gallbladders, 35 (95%) had carcinomatous peritonitis. Of the 28 patients with double-walled gallbladders, 23 (82%) had benign disease, such as liver cirrhosis (n = 22) and nephrotic syndrome with hypoalbuminemia (n = 1). The results of this study indicate that sonography is useful in determining whether the cause of ascites is malignant or benign disease.

Ascites↗

PubMed1991

Gallbladder varices: imaging findings in patients with portal hypertension.

A retrospective review of the medical and imaging records of 50 patients with portal hypertension examined in the authors' department during a 2-year period identified six patients with gallbladder wall varices. Imaging studies performed in these patients included computed tomography (CT) (four patients), duplex and color Doppler flow (five patients), and magnetic resonance (MR) (four patients). Five of six patients with gallbladder varices had portal vein thrombosis. Anechoic areas within the gallbladder wall detected with ultrasonography could be distinguished from intramural edema by using duplex or color Doppler flow imaging in all five patients in whom it was used. Contrast material enhancement of these varices was detected with CT in three patients, two of whom also had adjacent mesenteric collaterals. Gradient-echo MR imaging (fast imaging in steady precession/fast low-angle shot) showed flow-related enhancement within the gallbladder wall in two patients. The presence of gallbladder wall varices may imply the presence of portal vein thrombosis. Since these varices can be a source of major blood loss, surgeons must be made aware of them when operating on patients with portal hypertension.

Adult↗

PubMed1999

Expanded gallbladder fossa: simple MR imaging sign of cirrhosis.

PURPOSE: To determine the frequency on magnetic resonance (MR) images of a widened pericholecystic space, which the authors call the expanded gallbladder fossa sign, and to assess the sensitivity and specificity of this sign for cirrhosis. MATERIALS AND METHODS: Three-hundred thirteen patients who underwent MR imaging were included in this study, including 190 with pathologically proved cirrhosis (cirrhosis patients) and 123 without history of chronic liver diseases (control subjects). MR images were qualitatively evaluated by three independent observers for the presence of the expanded gallbladder fossa sign. This sign was considered present if there was enlargement of the pericholecystic space (i.e., gallbladder fossa) and the space was bounded laterally by the edge of the right hepatic lobe and medially by the edge of the left lateral segment, in conjunction with nonvisualization of the left medial segment. RESULTS: The expanded gallbladder fossa sign was seen in 129 cirrhosis patients and in three control subjects (P < .001). The sensitivity, specificity, accuracy, and positive predictive value of this sign for the MR diagnosis of cirrhosis were 68%, 98%, 80%, and 98%, respectively. CONCLUSION: The expanded gallbladder fossa sign on MR images is a frequently present, specific indicator of cirrhosis. This sign can be used as a simple and highly specific sign of cirrhosis, if present, despite the overall sensitivity of 68%.

Adult↗

PubMed2000

Pharmacology and modulation of K(ATP) channels by protein kinase C and phosphatases in gallbladder smooth muscle.

ATP-sensitive K(+) (K(ATP)) channels exhibit pharmacological diversity, which is critical for the development of novel therapeutic agents. We have characterized K(ATP) channels in gallbladder smooth muscle to determine how their pharmacological properties compare to K(ATP) channels in other types of smooth muscle. K(ATP) currents were measured in myocytes isolated from gallbladder and mesenteric artery. The potencies of pinacidil, diazoxide, and glibenclamide were similar in gallbladder and vascular smooth muscle, suggesting that the regions of the channel conferring sensitivity to these agents are conserved among smooth muscle types. Activators of protein kinase C (PKC), however, were less effective at inhibiting K(ATP) currents in myocytes from gallbladder than mesenteric artery. The phosphatase inhibitor okadaic acid increased the efficacy of PKC activators and revealed ongoing basal activation of K(ATP) channels by protein kinase A in gallbladder. These results suggest that phosphatases and basal kinase activity play an important role in controlling K(ATP) channel activity.

Adenosine Triphosphate↗

PubMed1977

Effects of cholecystokinin, gastrin, and related peptides on coho salmon gallbladder contraction in vitro.

UNLABELLED: Isometric contractions of coho salmon (Oncorhynchus kisutch) gallbladder longitudinal muscle strips were recorded in response to porcine cholecystokinin (CCK), octapeptide of CCK (OP-CCK), desulfated octapeptide of CCK (ds-OP-CCK), porcine heptadecapeptide gastrins I and II, and pentagastrin. Peak tonic contraction amplitude and peak rhythmic contraction frequency were used to construct concentration-response curves for each peptide. Observed maximal responses to each peptide were not significantly different; therefore, all peptides tested were equal in efficacy. CCK, OP-CCK, and gastrin II were equipotent, and ds-OP-CCK and gastrin I were equipotent. CONCLUSIONS: 1) porcine CCK can stimulate contraction of the coho salmon gallbladder; 2) tonic and rhythmic contractile responses are elicited in coho salmon gallbladder by agonists; 3) coho salmon gallbladder muscle cannot distinguish between agonists that differ in the location of a sulfated tyrosyl residue at position 6 versus position 7 from the C-terminus; and 4) the results of this study are consistent with the hypothesis that coho salmon gallbladder muscle contains a relatively primitive CCK receptor.

Acetylcholine↗

PubMed2005

Changes in guinea pig gallbladder smooth muscle Ca2+ homeostasis by acute acalculous cholecystitis.

Impaired smooth muscle contractility is a hallmark of acute acalculous cholecystitis. Although free cytosolic Ca2+ ([Ca2+]i) is a critical step in smooth muscle contraction, possible alterations in Ca2+ homeostasis by cholecystitis have not been elucidated. Our aim was to elucidate changes in the Ca2+ signaling pathways induced by this gallbladder dysfunction. [Ca2+]i was determined by epifluorescence microscopy in fura 2-loaded isolated gallbladder smooth muscle cells, and isometric tension was recorded from gallbladder muscle strips. F-actin content was quantified by confocal microscopy. Ca2+ responses to the inositol trisphosphate (InsP3) mobilizing agonist CCK and to caffeine, an activator of the ryanodine receptors, were impaired in cholecystitic cells. This impairment was not the result of a decrease in the size of the releasable pool. Inflammation also inhibited Ca2+ influx through L-type Ca2+ channels and capacitative Ca2+ entry induced by depletion of intracellular Ca2+ pools. In addition, the pharmacological phenotype of these channels was altered in cholecystitic cells. Inflammation impaired contractility further than Ca2+ signal attenuation, which could be related to the decrease in F-actin that was detected in cholecystitic smooth muscle cells. These findings indicate that cholecystitis decreases both Ca2+ release and Ca2+ influx in gallbladder smooth muscle, but a loss in the sensitivity of the contractile machinery to Ca2+ may also be responsible for the impairment in gallbladder contractility.

Acalculous Cholecystitis↗

PubMed2004

Characterization of intracellular Ca(2+) stores in gallbladder smooth muscle.

The existence of functionally distinct intracellular Ca(2+) stores has been proposed in some types of smooth muscle. In this study, we sought to examine Ca(2+) stores in the gallbladder by measuring intracellular Ca(2+) concentration ([Ca(2+)](i)) in fura 2-loaded isolated myocytes, membrane potential in intact smooth muscle, and isometric contractions in whole mount preparations. Exposure of isolated myocytes to 10 nM CCK caused a transient elevation in [Ca(2+)](i) that persisted in Ca(2+)-free medium and was inhibited by 2-aminoethoxydiphenylborane (2-APB). Application of caffeine induced a rapid spike-like elevation in [Ca(2+)](i) that was insensitive to 2-APB but was abolished by pretreatment with 10 muM ryanodine. These data support the idea that both inositol trisphosphate (IP(3)) receptors (IP(3)R) and ryanodine receptors (RyR) are present in this tissue. When caffeine was applied in Ca(2+)-free solution, the [Ca(2+)](i) transients decreased as the interval between Ca(2+) removal and caffeine application was increased, indicating a possible leakage of Ca(2+) in these stores. The refilling of caffeine-sensitive stores involved sarcoendoplasmic reticulum Ca(2+)-ATPase activation, similar to IP(3)-sensitive stores. The moderate Ca(2+) elevation caused by CCK was associated with a gallbladder contraction, but caffeine or ryanodine failed to induce gallbladder contraction. Nevertheless, caffeine caused a concentration-dependent relaxation in gallbladder strips either under resting tone conditions or precontracted with 1 muM CCK. Taken together, these results suggest that, in gallbladder smooth muscle, multiple pharmacologically distinct Ca(2+) pools do not exist, but IP(3)R and RyR must be spatially separated because Ca(2+) release via these pathways leads to opposite responses.

Animals↗

PubMed1981

Mechanical properties of primate gallbladder: description by a dynamic method.

Biomechanical theory was applied to devise a dynamic method for describing gallbladder tone in an in situ baboon model. Under pentobarbital sodium (Nembutal) anesthesia, cyclical infusion of bile into and withdrawal of bile from the gallbladder with continuous pressure monitoring allow instantaneous measurement of the pressure-volume ratio and thus of mean gallbladder compliance. This paper describes the method and details the manner of data analysis. Pharmacologic and hormonal agents with known gallbladder effects are used in order to demonstrate the sensitivity of the method. Pilocarpine, histamine, and cholecystokinin cause contraction of the primate gallbladder smooth muscle; this contraction is reflected in decreased compliance by continuous monitoring. Atropine administration results in increased ability to accommodate volume infusions; this effect has not been demonstrated by static monitoring in previous experiments. This new method allows continuous monitoring of compliance and offers both simplicity and sensitivity when compared with previous methods.

Animals↗

PubMed1984

Characterization of cholecystokinin receptors on bovine gallbladder membranes.

Cholecystokinin (CCK) binding to its receptors on a muscularis membrane fraction of bovine gallbladder was characterized using a biologically active CCK-33-[125I]Bolton-Hunter conjugate. Receptor binding was localized to the muscularis layer of the gallbladder; no binding was seen on either mucosal or serosal membranes. At 24 degrees C and pH 6.5, binding was maximal after 60-90 min of incubation, remained at a plateau for at least 240 min, and was reversed by the addition of unlabeled CCK-8. Optimal binding was seen at pH of 5.5 and required the presence of magnesium. Gallbladder binding data, best fit by a two-parameter model using a nonlinear least-squares computer program, was consistent with a single order of binding sites with a Kd of 618 +/- 168 pM and a binding capacity of 100.5 +/- 15.7 fmol/mg prot (mean +/- SE, n = 5). CCK-8 and CCK-33 inhibited 125I-CCK binding to gallbladder membranes with similar potencies, whereas desulfated CCK-8, gastrin I and II, and CCK-4 were at least 500 times less potent than CCK-33. The CCK antagonists dibutyryl cGMP and proglumide inhibited 125I-CCK binding with an IC50 of 31 and 600 microM, respectively. The present studies therefore demonstrate the existence of a specific CCK receptor on bovine gallbladder muscularis membranes with a high degree of selectivity for CCK analogues.

Animals↗

PubMed1985

Uptake and release of gamma-aminobutyric acid in guinea pig gallbladder.

The presence of gamma-aminobutyric acid (GABA)-ergic neuron in guinea pig gallbladder was investigated by measuring GABA contents and glutamate decarboxylase (GAD) activity and by demonstrating the uptake and release of [3H]GABA. GABA and GAD are both present in the gallbladder, and a positive correlation in regional distribution was observed among GABA, GAD, and the number of ganglion cells. The uptake of [3H]GABA by the gallbladder showed two saturable components; a high-affinity component (Km = 23.3 microM, Vmax = 7.63 nmol X g-1 X 10 min-1) and a low-affinity component (Km = 515 microM, Vmax = 57.1 nmol X g-1 X 10 min-1). These high-affinity and low-affinity transport systems corresponded to those obtained in the presence of beta-alanine and L-2,4-diaminobutyric acid, respectively, thereby suggesting the presence of neuronal and nonneuronal GABA transport systems in this tissue. Electrical transmural stimulation produced an increase in [3H]-GABA release from the isolated gallbladder preloaded with [3H]GABA, in the presence of beta-alanine. The stimulation-evoked release of [3H]GABA was prevented by calcium-free medium containing 1 mM EGTA and tetrodotoxin, thereby indicating that the released GABA originates from the nerve terminals. These results provide evidence for the presence of GABA-ergic neurons in the guinea pig gallbladder.

Animals↗

PubMed1990

Changes in tone of canine gallbladder measured by an electronic pneumatic barostat.

We developed an electronic pneumatic barostat to measure changes in gallbladder muscle tone in vivo independent of biliary flow dynamics. Dogs were prepared with a gallbladder cannula for insertion of barostat balloon and an inflatable balloon-occluder around the cystic duct. The barostat was validated to maintain a constant pressure of 2 +/- 0.4 (SE) mmHg within a plastic balloon of "infinite" compliance that filled the gallbladder lumen; changes in balloon volume reflected changes in wall tone because intraluminal pressure was kept constant. Gallbladder tone, as measured by the barostat balloon volume, varied cyclically with the duodenal migrating motor complex and decreased by 28 +/- 8% (P less than 0.05) at the time of phase III in the stomach and duodenum. Superimposed rapid changes in barostat volume occurred during phase III. The barostat response to motilin mimicked events during spontaneous phase III; in contrast, the response to cholecystokinin octapeptide (CCK-OP) was greater (volume decrease = 53 +/- 12%) and no phasic changes occurred. Two distinct patterns of gallbladder contraction were demonstrated: a basal tone increase with superimposed phasic contractions observed during phase III and after motilin, and a basal tone increase without phasic activity that occurs after CCK-OP.

Animals↗

PubMed1991

Monochloramine induces contraction of guinea pig gallbladder via two different pathways.

The purpose of the present investigation was to examine the effect and mechanism of action of the reactive oxygen metabolites monochloramine (NH2Cl), hypochlorous acid (HOCl), and hydrogen peroxide (H2O2) on gallbladder smooth muscle contractility. All oxidants caused concentration-dependent increases in resting tension of gallbladder muscle; the rank order of potencies (half-maximal concentration) was NH2Cl (30 microM) greater than HOCl (70 microM) greater than H2O2 (100 microM). The oxidant concentrations employed are those found to exist in inflamed tissue. Tetrodotoxin (0.5 microM) had no effect on gallbladder muscle contraction caused by the oxidants, suggesting a direct, nonneural action. The maximal response induced by NH2Cl, HOCl, or H2O2 was significantly (P less than 0.05) inhibited by 5 microM indomethacin and 5 microM piroxicam. The calcium channel blocker verapamil partially inhibited the contractile effect of NH2Cl but had no effect on the contraction induced by exogenous cyclooxygenase products. Monochloramine induced significant prostaglandin E2 release from the gallbladder, which was blocked by indomethacin. Furthermore, the effect of NH2Cl on the smooth muscle was blocked by 5-aminosalicylic acid (1 mM). We conclude that reactive oxygen metabolites induce contraction of gallbladder smooth muscle by a direct action. The effect is mediated via cyclooxygenase metabolites and activation of calcium influx.

Aminosalicylic Acids↗

PubMed1992

Convective movement of Ca2+ across guinea pig gallbladder epithelium.

Recently, much interest has developed in biliary calcium because of its importance in the pathogenesis and composition of gallstones. While much progress has been made in understanding the thermodynamic factors that control biliary calcium concentrations, little is known about the kinetic factors that control the movement of calcium across the gallbladder epithelium. These studies measure guinea pig gallbladder epithelial permeability to Ca2+ during in vivo convective water movement across the membrane. Water movement, ranging from -15.2 (absorption) to 6.3 microliters.min-1.cm-2 (water entry), was induced by placing hypotonic, isotonic, and hypertonic solutions into the gallbladder lumen. Calcium movement was found to be directly and linearly related to water flow, indicating that Ca2+ moved with the convective water flow, presumably across paracellular channels. The slope of this relationship (0.602), representing the concentration of calcium in the fluid translocated across the gallbladder epithelium, was only about half that of plasma or luminal contents, indicating that calcium movement across the membrane was restricted. The mean sieving coefficient (1 - r) of guinea pig gallbladder, calculated from this slope, was approximately 0.5, indicating that the epithelium is only moderately permeable to Ca2+. The results suggest that intraluminal chelation of Ca2+ for the possible prevention and/or treatment of calcium-containing gallstones is a potentially feasible therapeutic modality.

Animals↗

PubMed1994

PGE generates intracellular cAMP and accelerates mucin secretion by cultured dog gallbladder epithelial cells.

Mucin is the main secretory product of gallbladder epithelial cells. Increased gallbladder mucus secretion has been implicated in gallstone formation in humans. The mechanisms underlying control of mucin synthesis and secretion by the gallbladder are not known. This study aimed to elucidate the efficacy of a panel of secretagogues to stimulate mucin secretion and to determine the intracellular second messengers involved. Studies were carried out on normal well-differentiated epithelial cells from dog gallbladder grown in monolayer culture. Intracellular adenosine 3',5'-cyclic monophosphate (cAMP) as measured by radioimmunoassay increased in response to prostaglandin (PG) E2, PGE1, vasoactive intestinal peptide, epinephrine, and isoproterenol. The greatest effect, a 37-fold increase in cAMP level, was noted with PGE2 at 1.0 microM concentration. In contrast, three breakdown products of phosphatidylinositol (inositol triphosphate, inositol bisphosphate and inositol monophosphate) were not detected with any of the secretagogues tested. Assay of mucin secretion using tritiated N-acetyl-D-glucosamine, a mucin precursor, showed that the same secretagogues noted to increase intracellular cAMP led to an increase in mucin secretion. No correlation was noted, however, between the magnitude of the intracellular cAMP rise and the amount of mucin secreted. A membrane-permeable form of cAMP, dibutyryl cAMP, mimicked PGE2-induced mucin secretion. The results unequivocally show that secretagogue-stimulated mucin secretion in these normal gallbladder epithelial cells can proceed via a cAMP signal transduction pathway.

Animals↗

PubMed1998

Restoration by intratracheal gene transfer of bicarbonate secretion in cystic fibrosis mouse gallbladder.

Gallbladders from cystic fibrosis (CF) mice (Cftrtm1Cam and Cftrtm2Cam) were examined with the short-circuit current technique. The tissues failed to show any electrogenic anion transport in response to forskolin (cAMP stimulus) but responded to the Ca2+ ionophore ionomycin. Administration of the plasmid pTrial10-CFTR2 complexed with cationic liposomes (3beta-[N-(dimethylaminoethane)-carbamoyl]cholesterol and L-alpha-phosphatidylethanolamine dioleolyl) to the airways restored the phenotype of CF gallbladders to that of the wild type, but did not do so when given orally. Formation of human CFTR mRNA in gallbladders of transfected CF null mice was demonstrated. Using the reporter genes pCMV-luc and pCMV-LacZ, we showed that 1) the intratracheal route was more effective than the oral,intravenous, intramuscular, subcutaneous, or intraperitoneal routes in expressing luciferase activity in the gallbladder and 2) beta-galactosidase staining after pCMV-LacZ was confined to the columnar epithelium lining the gallbladder without any discernible activity in it smooth muscle. The discovery of an unusual route for gene transfer to the biliary system may give useful insight into counteracting the consequences of biliary fibrosis in human CF patients.

Animals↗