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PubMed1986

Ultrasonographic study of gallbladder motility during total parenteral nutrition.

Gallbladder sludge during total parenteral nutrition may be related to abnormal gallbladder motility. To test this hypothesis, gallbladder motility was assessed in 15 parenterally fed patients and in 22 controls using ultrasonography. Parenteral infusion was continuous in 10 cases and cyclic in 5 cases (6 PM to 10 AM). Gallbladder was simulated to a cone and gallbladder volume was calculated after ultrasonographic measurement of the greatest length and diameter. Six to 12 gallbladder volume measurements were performed between 8 AM and 11 PM in the parenteral nutrition group. In controls gallbladder volume was measured hourly between 8 AM and 8 PM. Thus maximal diurnal gallbladder volume and maximal diurnal gallbladder emptying, expressed as a percentage of maximum gallbladder volume, were determined. Maximal gallbladder volume was identical in the two groups. Gallbladder emptying was significantly reduced in parenterally fed patients (p less than 10(-9)) during both continuous and cyclic infusion.

Adolescent↗

PubMed1991

Inhibition of prostaglandin synthesis fails to prevent gallbladder mucin hypersecretion in the cholesterol-fed prairie dog.

Gallstone formation in the cholesterol-fed prairie dog is preceded by an increase in mucin secretion by the gallbladder epithelium, and mucin hypersecretion is believed to promote cholesterol gallstone formation by accelerating the nucleation of cholesterol monohydrate crystals. Some studies have suggested that gallbladder mucin hypersecretion is mediated by increases in gallbladder prostaglandin synthesis, but other observations are difficult to reconcile with this view. An organ culture technique was used to measure mucin secretion in normal prairie dog gallbladder in response to exogenous prostaglandins and agents that increased or decreased endogenous prostaglandin production. Incubation with indomethacin produced a concentration-dependent inhibition of endogenous prostaglandin synthesis with virtually complete inhibition at 10(-5) mol/L indomethacin. However, indomethacin had no effect on gallbladder mucin secretion at concentrations as high as 10(-5) mol/L, and significant inhibition of mucin secretion was only found at 10(-4) mol/L indomethacin, a concentration that also produced a significant increase in lactate dehydrogenase release from cultured explants. Incubation of gallbladder explants with the calcium ionophore A23187 significantly stimulated endogenous prostaglandin synthesis in a concentration-dependent manner, increasing synthesis of prostaglandins E and F to as much as 278% +/- 20% and 335% +/- 21% of basal values, respectively; however, the same concentrations of A23187 did not stimulate mucin secretion. Incubation of gallbladder explants in the presence of exogenous prostaglandin E2 or prostaglandin F2a in concentrations as high as 10(-6) mol/L also did not stimulate mucin secretion. Prairie dogs fed a lithogenic 1.2% cholesterol diet showed a significant increase in gallbladder mucin secretion after 1 week (117.5 +/- 10.2% of control, P less than 0.05), and 4 of 5 had formed cholesterol monohydrate crystals after 3 weeks. Long-term treatment with indomethacin, 1.2 mg.kg-1.day-1, failed to inhibit gallbladder mucin hypersecretion (129.2 +/- 10.7% of control after 1 week) or cholesterol monohydrate crystal formation (3/5) in cholesterol-fed prairie dogs. Furthermore, incubation of explants with 10(-5) mol/L indomethacin failed to prevent in vitro mucin hypersecretion in cholesterol-fed animals. These findings suggest that prostaglandins do not regulate gallbladder mucin secretion in the prairie dog, and it is unlikely that increases in gallbladder prostaglandin synthesis are responsible for mediating gallbladder mucin hypersecretion during cholelithiasis in the prairie dog.

Animals↗

PubMed1994

Increased intragallbladder pressure stimulates gallbladder eicosanoid release.

The stimulus for increased gallbladder eicosanoid synthesis during cholecystitis is unknown. This study examines the hypothesis that increased intragallbladder pressure stimulates endogenous gallbladder eicosanoid release. Rabbit gallbladders were perfused in vitro at 1 ml/minute with oxygenated Krebs-Henseleit buffer and subjected to 0, 12 or 24 mm Hg of intraluminal gallbladder pressure. Release of 6-keto-PGF1 alpha infinity PGE2 and thromboxane B2 were measured in all groups after 15 and 30 and 60 minutes of perfusion by enzyme immunoassay and gallbladders were examined histologically. Increasing intraluminal gallbladder pressure concomitantly increased gallbladder 6-keto-PGF1 alpha release 2 fold or more at all time of perfusion and altered gallbladder mucosal architecture by increasing basolateral edema in the submucosal space. Infusion of indomethacin (10 micrograms/ml in the perfusion media) decreased 6-keto-PGF1 alpha release from the in vitro perfused gallbladders subjected to 24 mm Hg by 70%. Increased gallbladder eicosanoid release during early cholecystitis may in part be related to the physical force of increased gallbladder intraluminal pressure on the gallbladder mucosa.

6-Ketoprostaglandin F1 alpha↗

PubMed2006

Pioglitazone increases gallbladder volume in insulin-resistant obese mice.

BACKGROUND: Both obesity and diabetes are associated with an increased incidence of gallstones. Recent animal and human data from our laboratory suggest that insulin resistance is associated with increased gallbladder volume and/or impaired gallbladder emptying. Pioglitazone is a thiazolidinedione that has been shown to improve insulin resistance. Therefore, we tested the hypothesis that pioglitazone would improve insulin resistance, decrease resting gallbladder volume and improve gallbladder response to neurotransmitters in insulin-resistant obese mice fed a 25% carbohydrate diet. MATERIALS AND METHODS: Twenty eight-week-old insulin-resistant obese (Lep(ob)) mice fed a 25% carbohydrate diet for 4 weeks. Half of the animals had 0.3 g/kg pioglitazone added to their diet. At 12 weeks all animals were fasted and underwent cholecystectomy. Gallbladder volume and weight were measured, and fresh gallbladders were placed in a muscle bath to assess response to acetylcholine (ACh 10(-5)M), neuropeptide Y (NPY 10(-8,-7,-6)M) and cholecystokinin (CCK 10(-10,-9,-8,-7)M). Serum glucose and insulin were measured, and HOMA Index, a measure of insulin resistance, was calculated. RESULTS: Fasting serum insulin and HOMA Index were significantly decreased (P < 0.03), but gallbladder volume was significantly increased (P < 0.03) in the pioglitazone treated group. Pioglitazone did not alter gallbladder weight or response to ACh, NPY, or CCK. CONCLUSION: These data suggest that in insulin-resistant obese mice pioglitazone 1) lowers insulin-resistance, 2) increases resting gallbladder volume, and 3) does not alter gallbladder response to neurotransmitters. Therefore, we conclude that pioglitazone, while improving insulin resistance, paradoxically increases gallbladder volume and, thereby, may increase the propensity for gallstone formation by enhancing gallbladder stasis.

Acetylcholine↗

PubMed2005

Protein kinase C-alpha regulation of gallbladder Na+ transport becomes progressively more dysfunctional during gallstone formation.

Gallbladder Na+ absorption and biliary Ca2+ are both increased during gallstone formation and may promote cholesterol nucleation. Na+/H+ exchange (NHE) is a major pathway for gallbladder Na+ transport. Ca2+-dependent second messengers, including protein kinase C (PKC), inhibit basal gallbladder Na+ transport. Multiple PKC isoforms with species- and tissue-specific expression have been reported. In this study we sought to characterize Ca2+-dependent PKC isoforms in gallbladder and to examine their roles in Na+ transport during gallstone formation. Gallbladders were harvested from prairie dogs fed either nonlithogenic chow or 1.2% cholesterol-enriched diet for varying periods to induce various stages of gallstone formation. PKC was activated with the use of phorboldibutyrate, and we assessed gallbladder NHE regulation by measuring unidirectional Na+ flux and dimethylamiloride-inhibitable 22Na+ uptake. We measured gallbladder PKC activity with the use of histone III-S phosphorylation and used Gö 6976 to determine PKC-alpha contributions. Gallbladder PKC isoform messenger RNA and protein expression were examined with the use of Northern- and Western-blot analysis, respectively. Prairie dog and human gallbladder expresses PKC-alpha, betaII, and delta isoforms. The PKC activation significantly decreased gallbladder J(Na)(ms) and reduced baseline 22Na+ uptake by inhibiting NHE. PKC-alpha mediated roughly 42% of total PKC activity under basal conditions. PKC-alpha regulates basal gallbladder Na+ transport by way of stimulation of NHE isoform NHE-2 and inhibition of isoform NHE-3. PKC-alpha blockade reversed PKC-induced inhibition of J(Na)(ms) and 22Na+ uptake by about 45% in controls but was progressively less effective during gallstone formation. PKC-alpha contribution to total PKC activity is progressively reduced, whereas expression of PKC-alpha mRNA, and protein increases significantly during gallstone formation. We conclude that PKC-alpha regulation of gallbladder NHE becomes progressively more dysfunctional and may in part account for the increased Na+ absorption observed during gallstone formation.

Animals↗

PubMed1999

Does endoscopic papillary balloon dilation affect gallbladder motility?

BACKGROUND: Endoscopic papillary balloon dilation for treatment of bile duct stones is likely to preserve papillary function. However, endoscopic papillary balloon dilation may affect gallbladder motility. We investigated the effects of endoscopic papillary balloon dilation on gallbladder motility. METHODS: Ten patients with an intact gallbladder (six with and four without gallbladder stones) who underwent endoscopic papillary balloon dilation for choledocholithiasis were studied. Gallbladder motility was examined before and 7 days and 1 month after endoscopic papillary balloon dilation. Gallbladder volume, while fasting and after dried egg yolk ingestion, was determined by ultrasonography. RESULTS: Before endoscopic papillary balloon dilation, particularly in patients with gallbladder stones, the gallbladder showed significantly larger fasting volume and lower yolk-stimulated maximum contraction compared with control subjects. Seven days after endoscopic papillary balloon dilation, fasting volume was decreased and maximum contraction was increased, regardless of the presence of gallbladder stones, with significant differences from the values before endoscopic papillary balloon dilation. One month after endoscopic papillary balloon dilation, these changes were reduced and gallbladder function did not differ significantly from baseline. CONCLUSIONS: After endoscopic papillary balloon dilation, gallbladder motility improves transiently at 7 days but returns to baseline at 1 month. In terms of gallbladder motility, endoscopic papillary balloon dilation does not seem to increase the subsequent risk of acute cholecystitis.

Aged↗

PubMed2003

Gallbladder motility in agouti-yellow and leptin-resistant obese mice.

BACKGROUND: Obesity is a polygenic disorder that is associated with gallstone disease. We have previously shown that leptin deficiency in obese mice correlates with decreased gallbladder motility, suggesting that leptin plays a role in the link between gallstone disease and obesity. However, most obese humans are leptin-resistant, and relatively few are leptin-deficient. To confirm that leptin dysfunction is responsible for impaired gallbladder motility in obese mice, we hypothesized that leptin-resistant obese mice (Lep(db)) would have abnormal gallbladder motility while obese mice with intact leptin function (Agouti Yellow, A(y)) would have normal gallbladder motility. MATERIALS AND METHODS: Eighteen lean control (C57BL/6J), 10 A(y) and 12 Lep(db) female mice were fasted overnight, weighed, and livers and gallbladders were harvested. Liver weights and gallbladder volumes were measured. Gallbladder contractile responses (N/cm(2)) to acetylcholine (10(-5)M), neuropeptide Y (10(-8,-7,-6) M) and cholecystokinin (10(-10,-9,-8,-7)M) were determined in muscle bath chambers. Results were analyzed by analysis of various (ANOVA) and with the Mann-Whitney Rank Sum Test. RESULTS: Both Agouti yellow (A(y)) and leptin-resistant (Lep(db)) obese mice had body weights, liver weights and gallbladder volumes that were significantly greater (P < 0.01) than lean control mice. Leptin-resistant obese mice had gallbladder responses to acetylcholine, neuropeptide Y and cholecystokinin that were significantly less (P < 0.01) than both lean control and Agouti yellow obese mice. CONCLUSIONS: These data suggest that (1). leptin-resistant obese mice (Lep(db)) have abnormal gallbladder motility and (2). obese mice with normal leptin metabolism (A(y)) have normal gallbladder response to neurotransmitters. We conclude that leptin represents a link between obesity, gallbladder motility and gallstone formation.

Acetylcholine↗

PubMed2000

Differential effect of prostaglandins on gallstone-free and gallstone-containing human gallbladder.

Nonsteroidal antiinflammatory drugs, inhibitors of prostaglandin synthesis, have different effects on gallbladder contractility in normal and diseased human gallbladders in vivo. We investigated this differential effect by comparing the effects of prostaglandins PGE2 and PGF2alpha, the thromboxane A2 mimetic U46619, and PGI2 on in vitro contractility in gallstone-free and gallstone-containing human gallbladders. Isometric tension was measured in gallbladder muscle strips mounted in organ baths. EC50 was calculated for each agonist. The rank order of potency in gallstone-free gallbladders was PGE2 > CCK > U46619 > PGF2alpha and in gallstone-containing gallbladders was U46619 > PGE2 > CCK > PGF2alpha. PGI2 produced contraction of gallstone-free gallbladder and relaxation of gallstone-containing gallbladder in the basal state. Further, PGI2 produced no relaxation in gallstone-free muscle strips precontracted with CCK, but significant relaxation in CCK precontracted gallstone-containing strips. PGE2, PGF2alpha, and U46619 are potent contractors of gallstone-free and gallstone-containing gallbladders, whereas PGI2 relaxes only gallstone-containing gallbladders. Since gallbladders containing cholesterol-supersaturated bile produce increased PGI2, this PGI2-induced relaxation may be a determinant of the impaired gallbladder motility of gallstone disease.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1982

Ischaemic cholecystitis and infarction of the gallbladder.

The clinicopathological features of forty three patients with gallbladder disease are presented where ischaemia appeared to be the primary aetiological factor. Histopathological changes of severe ischaemia (ischaemic cholecystitis) were present in 16 patients and of infarction of the gallbladder in the remaining 27 patients. All patients with ischaemic cholecystitis and 19 of the patients with infarction of the gallbladder had a thick walled gallbladder due to a serosal reaction, and these 35 gallbladders all contained calculi. The remaining eight patients with infarction of the gallbladder had a thin walled gallbladder without serosal reaction. Only two of these patients had gallbladders that contained calculi. The pathogenesis of thick walled ischaemic cholecystitis or infarction appeared to be related to intramural vascular insufficiency which accompanies calculus disease of the gallbladder. Thin walled infarction of the gallbladder appeared to develop as a result of extramural arterial insufficiency due to arterial disease, thrombosis or trauma. The clinical course of thick walled ischaemic gallbladder disease was not significantly different from severe acute cholecystitis with calculi. However, 75% of the patients with thin walled infarcted gallbladders were severely ill from their associated illness or trauma, and nearly all died.

Adult↗

PubMed2000

Primary gallbladder cancer: recognition of risk factors and the role of prophylactic cholecystectomy.

The objective of this article is to review the available literature on the epidemiology, predisposing factors, and conditions associated with primary gallbladder cancer, and to discuss the role of prophylactic cholecystectomy in high-risk patient populations. Gallbladder cancer is a highly malignant tumor with a poor 5-yr-survival rate. It is a tumor of the elderly and has striking genetic, racial, and geographic characteristics, with an extremely high prevalence in Native Americans and Chileans. Cholelithiasis is a well-established risk factor for gallbladder cancer and the risk seems to correlate with stone size. Polyps that are >1 cm, single, sessile, and echopenic are associated with a higher risk of malignancy. Anomalous junction of pancreaticobiliary ducts (AJPBD), especially without choledochal cyst, and porcelain gallbladder are additional factors that predispose to gallbladder cancer. Lesser associations include chronic bacterial infections of the gallbladder, typhoid carrier state, certain occupational and environmental carcinogens, hormonal changes in women, and certain social, dietary, and familial factors. It is important to identify high-risk groups for gallbladder cancer because of the dismal nature of this tumor. In patients with porcelain gallbladder and anomalous junction of the pancreatic and biliary ducts, cholecystectomy is recommended provided that the patient is a good operative candidate. Patients with large solitary polyps or gallstones require close ultrasonic follow-up. With the advent of endoscopic ultrasound it is expected that early changes of malignancy in polyps will be reliably detected, and more patients will potentially be cured with a simple cholecystectomy. Through a MEDLINE/PAPERCHASE search we identified and reviewed articles regarding gallbladder cancer published in English-language journals between 1966 and 1999, using the key words biliary tract and gallbladder diseases, cancer, neoplasms, surgery, cholelithiasis, gallstones, cholecystitis, gallbladder polyps, risk factors, chemical industry, occupational diseases, typhoid, porcelain gallbladder, bacteremia, and precancerous conditions. We also used the bibliography of relevant articles to increase our search. A total of 122 publications were selected using the mentioned data source.

Cholecystectomy↗

PubMedDate not supplied

Ultrasonographic evaluation of gallbladder wall thickness in cats.

Ultrasonography of the gallbladder and biliary tract was performed on 42 cats: 22 clinically healthy cats (group A) and 20 cats with hepatobiliary disease and post mortem confirmation of gallbladder abnormalities (group B). The gallbladder wall was visible in 9 of 22 cats in group A and all 20 cats in group B. Additional gallbladder findings in group B included shape anomalies, biliary tract obstruction, wall thickening, polyps, neoplasia, and biliary sludge. Ultrasonographic evaluation of abdominal organs identified pancreatic disease as the predominant pathological cause of extrahepatic biliary obstruction. Hepatic parenchymal involvement was noted with inflammation and thickening of the gallbladder wall. Histologically, gallbladder walls were characterized by mucous gland hyperplasia, inflammation, infiltration, edema, epithelial detachment, and/or neoplasia. Ultrasonographic and histologic gallbladder wall measurements of 20 cats in group B agreed within 0.4 mm and all cats with a gallbladder wall thickness > or =1.0 mm had histopathologic abnormalities of the wall. Serum biochemical analysis revealed elevations of one or more parameters in all cats of group B, but was non-specific for a gallbladder lesion. The results of this study indicate that a visible, echogenic gallbladder wall can be considered a normal variant and is not always associated with hepatobiliary disease. Ultrasonography is accurate in measuring gallbladder wall thickness. Wall thickness greater than 1 mm is accurate in predicting gallbladder disease in cats, while a thickness less than 1 mm cannot rule out mild or chronic inflammation.

Animals↗

PubMed1991

Effect of two new cholecystokinin antagonists on gallbladder emptying in opossums.

In this investigation we evaluated the effect of two new cholecystokinin (CCK) antagonists, CR 1409 and L364,718, on gallbladder emptying in the opossum. Gallbladder emptying was elicited by both exogenous and endogenous CCK. The three test challenges were 1) intravenous infusion of CCK octapeptide (OP) (10 ng.kg-1.min-1), 2) feeding, and 3) intraduodenal infusion of Isocal (0.4 ml/min), a fat-containing nutrient. During control conditions each test challenge elicited approximately 60% gallbladder emptying within 30 min and 70% emptying by 60 min. At given doses both CR 1409 and L364,718 substantially antagonized or abolished the gallbladder emptying elicited by each of the test challenges. The antagonism for postprandial gallbladder emptying was diminished between 30 and 50 min compared with that for CCK-OP infusion and intraduodenal infusion of Isocal. Unexpectedly, the gallbladder emptying induced by infusion of motilin (5 micrograms.kg-1.h-1) was antagonized by either CR 1409 or L364,718. In anesthetized animals, gallbladder contraction was induced by a variety of agonists, such as bethanechol, histamine phosphate, 5-hydroxytryptamine, and phenylephrine. In this later model CR 1409 and L364,718 functioned solely as selective antagonists. We conclude that for the opossum gallbladder 1) the CCK antagonists CR 1409 and L364,718 antagonize or abolish gallbladder emptying induced by exogenous or endogenous CCK; 2) the pattern of CCK antagonism after feeding suggests that the early phase of postprandial gallbladder emptying is mediated by a mechanism other than endogenous CCK, whereas late postprandial emptying is mediated by release of endogenous CCK; and 3) CR 1409 and L364,718 are not totally specific antagonists for gallbladder CCK receptors alone but also antagonize gallbladder contraction induced by motilin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Responses of primate T1-T5 spinothalamic neurons to gallbladder distension.

Extracellular unit recordings were obtained from 44 spinothalamic tract (STT) neurons in the T1-T5 segments of 15 alpha-chloralose anesthesized monkeys (Macaca fascicularis). Each cell had a somatic receptive field in the left chest region and was excited by electrical stimulation of cardiopulmonary sympathetic afferent fibers. Gallbladder distension to pressures between 20 and 100 mmHg increased activity in 16 of 44 neurons. Responses usually consisted of bursts of activity associated with increased gallbladder pressure (phasic responses) followed by maintained activity during the distension (tonic responses). Magnitude of phasic responses was linearly related to the distending pressure and was consistently greater than magnitude of tonic responses. The gallbladder-responsive and nonresponsive groups included similar proportions of wide dynamic range, high threshold, and high-threshold inhibitory cells. Nine of 10 gallbladder-responsive cells and 11 of 21 gallbladder-nonresponsive cells increased their discharge rate after injection of 2 micrograms/kg bradykinin into left atrium. Activity of cells with gallbladder input increased from 14 +/- 4 to 33 +/- 4 spikes/s. Cells without gallbladder input increased their discharge rate to a significantly less degree (10 +/- 3-23 +/- 4 spikes/s). These results indicate that upper thoracic STT neurons may increase their activity during gallbladder distension. Convergence of afferent information from the chest and gallbladder may explain chest pain occurring during gallbladder disease. Furthermore the tendency of gallbladder-responsive cells to respond to bradykinin injections with a high rate of discharge could explain how this chest pain of gallbladder origin may closely mimic pain of angina pectoris.

Angina Pectoris↗

PubMedDate not supplied

Mucin content in gallbladders with brown pigment stones or combination stones with a brown periphery.

BACKGROUND/AIMS: Gallbladder mucus itself has been recognized to play an important role in gallstone development. Despite the diverse mechanisms of stone induction and the differences in stone composition, there is a quantitative increase in the epithelial mucus production period before stone formation. As brown pigment stones are found frequently in gallstone disease, we conducted a study on gallbladders with brown pigment stones or combination stones with a brown periphery to evaluate the mucin content in the gallbladder epithelium in comparison to gallbladders with cholesterol stones and those without stones. METHODS: Gallbladder specimens were fixed in 10% formalin immediately after cholecystectomy and then embedded in paraffin. The specimens were sectioned for periodic acid-Schiff-alcian blue (PAS-AB, pH 2.5) double stain to evaluate the intra-epithelial mucin content. The PAS-AB index was calculated as a proportion of the PAS-AB-positive mucin area to the total epithelial area, using a computerized image analyzer. RESULTS: Evaluation of the PAS-AB index on the lining epithelia of gallbladders showed that it was 32.43 +/- 9.96% in gallbladders with brown stones, which is significantly (p < 0.001) higher than in gallbladders with cholesterol stones (15.63 +/- 6. 75%) and gallbladders without stones (9.55 +/- 4.77%). CONCLUSION: The results show that gallbladders with brown stones contain more abundant mucin than gallbladders with cholesterol stones or those without stones. They also suggest that the gallbladder epithelium per se might play a more important role in stone formation in those with brown stones than in those with cholesterol stones.

Adult↗

PubMed2003

Keratin-8 null mice have different gallbladder and liver susceptibility to lithogenic diet-induced injury.

Keratin transgenic mouse models and the association of human keratin mutations with liver disease highlight the importance of keratins in protecting the liver from environmental insults, but little is known regarding keratins and their function in the gallbladder. We characterized keratin expression pattern and filament organization in normal and keratin polypeptide-8 (K8)-null, K18-null and K19-null gallbladders, and examined susceptibility to liver and gallbladder injury induced by a high-fat lithogenic diet (LD) in K8-null mice. The major keratins of normal mouse gallbladder are K8>K19>K18 which become markedly depleted in K8-null mice with minor K18/K19 remnants and limited K7 over-expression. Compensatory K18/K20 protein and RNA overexpression occur in K19-null but not in K18-null gallbladders, probably because of the higher levels of K19 than K18 in normal gallbladder. LD challenge causes more severe liver injury in K8-null than wild-type mice without altering keratin protein levels. In contrast, wild-type and K8-null gallbladders are equally susceptible to LD-induced injury and stone formation, but wild-type gallbladders do overexpress keratins upon LD challenge. LD-induced injury triggers keratin hyperphosphorylation in wild-type livers and gallbladders. Hence, mouse gallbladder K8/K18/K19 expression is induced in response to cholelithiasis injury. A high-fat LD increases the susceptibility of K8-null mice to liver but not gallbladder injury, which suggests that keratin mutations may increase the risk of liver damage in patients with steatohepatitis. Differences between K8-null mouse gallbladder and hepatocyte susceptibility to injury may be related to their minimal versus absent keratin expression, respectively.

Animals↗

PubMed1991

Studies on the intramural nerves of the hamster and mouse gallbladders.

We first carried out microscopic observation of the intramural nerves of hamster and mouse gallbladders which were fixed and stained with a solution of OsO4 and ZnI2. For this microscopic observation, the guinea-pig gallbladder was used as a control. We then investigated the relationship between the motility and intramural nerves of the isolated gallbladder in both the hamster and mouse. The following results were obtained: 1. The ganglionated plexus and the perivascular nerves as the intramural nerves of the guinea-pig gallbladder were observed in the subserosal layer. These perivascular nerves were not possessed of ganglia. On the other hand, the nerve plexus and the perivascular nerves as the intramural nerves of the gallbladders of hamster and mouse were observed in the subserosal layer. These nerves, that is, the nerve plexus and the perivascular nerves, were not possessed of ganglia. That is to say, no ganglionated plexus or ganglia were observed in the subserosal layer of the walls of hamster and mouse gallbladders. 2. The isolated hamster and mouse gallbladders evoked spontaneous motility. This spontaneous motility was little affected by either atropine (1 x 10(-6) M) or tetrodotoxin (1 x 10(-7) M). 3. The hamster and mouse gallbladders showed a contractile response to electrical stimulation with rectangular pulses (50 volt, 40 Hz) of durations of 0.5, 1, 2, 3, 4, 5 or 6 msec for a period of 10 sec. These contractile responses were little affected by either atropine (1 x 10(-6) M) or tetrodotoxin (1 x 10(-7) M). 4. The long duration of the contractile response was mediated by electrical stimulation with rectangular pulses (50 volt, 40 Hz) of durations of 4, 5 or 6 msec for a period of 10 sec. That is to say, its duration time was approximately from 8 to 15 minutes for both hamster and mouse. These results suggest that the hamster and mouse gallbladders may not contain the nerves that take part in the movement of the gallbladder. That is to say, the contractile response of the hamster and mouse gallbladders seems to be myogenic rather than neurogenic in its control. It is, however, possible that some substance other than the neurotransmitter in the walls of these gallbladders may also play a part in the control of the contractile response, although further study will be necessary to verify this suggestion.

Animals↗

PubMed1991

Altered gallbladder contractility after extracorporeal shock-wave cholecystolithotripsy.

Change in gallbladder contractility after biliary extracorporeal shock-wave lithotripsy (ESWL) may significantly influence the clearance of fragments after successful gallstone fragmentation. We assessed changes in gallbladder contractility in response to an oral fatty meal in 50 patients 1 month after biliary ESWL (all fragments were smaller than 3 mm) and also in a separate group of 10 patients 3 months after complete clearance of fragments. The prevalence of persistent lumen-obliterating contraction of the gallbladder after biliary ESWL also was analyzed in 325 patients. Gallbladder contractility remained unchanged in 30, increased in nine, and decreased in 11 of the 50 patients. The average reduction in the fasting gallbladder volume after lithotripsy was 28% (p less than .001). Gallbladder contractility remained unchanged 3 months after complete clearance of fragments in six of 10 patients studied separately. A decrease (n = 2) or increase (n = 2) in contractility was seen in the remaining patients. No significant difference occurred in the average ejection fraction of the gallbladder before lithotripsy and after complete clearance of the fragments. Thirty-four of the 325 patients who have so far undergone biliary ESWL had a completely contracted gallbladder with no lumen visible on sonography. The gallbladder returned to a relaxed state in half of these patients within 1-9 months. Thus, biliary ESWL did not significantly alter gallbladder contractility in 60% of patients. A significant reduction in the volume of the fasting gallbladder occurred after lithotripsy. Successful clearance of fragments did not improve the contractility of stonebearing gallbladders in the majority of patients.

Cholecystokinin↗

PubMed2000

Prevalence and significance of gallbladder abnormalities seen on sonography in intensive care unit patients.

OBJECTIVE: We evaluated sonographic abnormalities of the gallbladder other than acalculous cholecystitis across a broad range of intensive care unit (ICU) patients. SUBJECTS AND METHODS: Fifty-five consecutive patients (age range, 18-94 years old; mean age, 56 years; 33 men, 22 women), who were admitted to the ICU with a variety of diagnoses, underwent sonography of the gallbladder twice a week. Patients with gallbladder calculi were excluded from the study. The gallbladder was examined for the recognized sonographic features of acalculous cholecystitis: gallbladder wall thickening, gallbladder distention, intramural gallbladder lucencies (striated gallbladder wall), pericholecystic fluid, gallbladder sludge, and Murphy's sign. These findings were correlated with clinical and laboratory parameters that are associated with acalculous cholecystitis: fever, WBC, liver function tests, levels of serum bilirubin, mechanical ventilation status, and administration of parenteral nutrition, narcotic analgesics, antibiotics, and pressor agents. RESULTS: Eleven of the 55 patients were found to have gallbladder calculi and were excluded from the study. Thirty-seven (84%) of the remaining 44 patients had at least one sonographic abnormality while in the ICU. Twenty-five (57%) of the 44 patients had as many as three abnormalities found on sonography, and six (14%) of 44 patients had four or five sonographic findings of gallbladder abnormalities while in the ICU. No statistically significant correlation was found among any of these sonographic abnormalities and the clinical and laboratory parameters. CONCLUSION: Gallbladder abnormalities are frequently seen on sonography in ICU patients, even if these patients are not suspected of having acalculous cholecystitis; therefore, sonography appears to be of limited value in diagnosing acalculous cholecystitis in ICU patients.

Adolescent↗