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PubMed1995

Influence of ceruletid on gallbladder contraction: a possible prophylaxis of acute acalculous cholecystitis in intensive care patients?

The purpose of this study was to investigate the utility of repeated applications of ceruletid to reduce gallbladder volume and its feasibility as a means of prophylaxis of acute acalculous cholecystitis in intensive care patients. First, a dose-response curve of ceruletid was obtained in 20 mechanically ventilated patients of a surgical intensive care unit (SICU) not receiving enteral nutrition. An effective dose of ceruletid, defined by a 50% reduction of gallbladder volume was established and subsequently studied in 40 mechanically ventilated SICU patients on total parenteral nutrition in a prospective, randomized, controlled, triple-blind trial. Gallbladder volume, sludge formation and side effects were evaluated. A dose of 1.5 micrograms/kg body weight ceruletid was established as the effective dose, causing 50% reduction of gallbladder volume in all patients studied and reduction of gallbladder sludge in 95%. In 67.5% of patients side effects were observed, requiring therapeutic intervention in 68%. It is concluded that ceruletid is effective in stimulating gallbladder contraction and reducing sludge formation in severely ill patients on intensive care units. Its routine use as prophylaxis of acute acalculous cholecystitis, however, may be limited by the nature, severity and frequency of side effects.

Acute Disease↗

PubMed1987

Ultrasonographic identification of the human fetal gallbladder in utero.

Ultrasonographic studies of the human fetal gallbladder were performed in utero on 149 fetuses ranging from 20 to 39 weeks of gestation. The gallbladder could be identified in 37.5% (20-23 weeks) to 64.7% (24-27 weeks) after 20 weeks of gestation. The normal sonographic characteristics of the fetal gallbladder were described and the area of fetal gallbladder, the length and the width were measured, respectively. The ultrasonographic identification of the fetal gallbladder is a first step in antenatal detection of congenital anomalies affecting the gallbladder.

Female↗

PubMed1996

Reflex coronary vasoconstriction caused by gallbladder distension in anesthetized pigs.

BACKGROUND: Gallbladder distension in anesthetized pigs reflexly increases heart rate and arterial pressure by means of afferent vagal pathways and efferent sympathetic mechanisms. The effect of such distension on the coronary circulation is unknown. The present study was undertaken to determine whether gallbladder distension primarily causes reflex changes in left circumflex blood flow. METHODS AND RESULTS: In 21 pigs anesthetized with sodium pentobarbitone (16) or alpha-chloralose (5), left circumflex blood flow was measured with an electromagnetic flowmeter. A balloon positioned within the gallbladder was distended with volumes of Ringer's solution equal to the volumes of bile previously withdrawn (mean vol: 62 mL; mean gallbladder pressure: 12 mm Hg). Heart rate and arterial pressure were kept constant by atrial pacing and by a pressurized reservoir connected to the left femoral artery. Gallbladder distension always caused a decrease in circumflex blood flow. In 6 of the 16 sodium pentobarbitone-anesthetized pigs, this decrease was graded by step increments of distension. In 5 of these 16 pigs, the decrease in circumflex blood flow was not affected by atropine. In 10 of these 16 pigs, including those given atropine, the response was not affected by propranolol but was abolished by subsequently giving phentolamine. Cervical vagotomy abolished the coronary vasoconstriction in the remaining 6 pigs. In the 5 alpha-chloralose-anesthetized pigs, the response was not significantly affected by cutting the splanchnic nerves but was abolished by subsequent cervical vagotomy. CONCLUSIONS: The present study showed that innocuous distension of the gallbladder in anesthetized pigs caused a reflex coronary vasoconstriction that involved efferent sympathetic mechanisms related to alpha-adrenoceptors and afferent vagal pathways.

Adjuvants, Anesthesia↗

PubMed1973

Interactions between intraluminal bile acids and digestive products on pancreatic and gallbladder function.

Interactions between bile acids (taurocholate, TC; taurochenodeoxycholate, TCDC; or taurodeoxycholate, TDC) and digestive products (essential amino acids, EAA or monoolein, MO) in the lumen of the proximal small bowel, affecting pancreatic enzyme secretion and gallbladder contraction, were studied in 77 healthy volunteers by a perfusion method. Perfusion of EAA or MO caused significant increases in pancreatic enzyme output together with gallbladder contraction; MO was more potent and induced enzyme outputs comparable to the maximal response attained with intravenous cholecystokinin-pancreozymin (CCK-PZ). Perfusion of TC alone had no effect, but addition of 10 mM of either TC, TCDC, or TDC to perfusates containing EAA, or 10 mM TC to MO, or both significantly reduced pancreatic enzyme output and prevented gallbladder contraction. A lower concentration of TC (5 mM) added to EAA also produced a significant inhibitory effect. Inhibition of the stimulatory action of digestive products occurred in the jejunum as well as in the duodenum. The inhibitory action of bile acid was considered to be intraluminal since (a) bile acid did not modify the effects of CCK-PZ given intravenously; and (b) the stimulatory effect of digestive products perfused in the duodenum on pancreatic and gallbladder function was not influenced by simultaneous perfusion of bile acid in the jejunum. It is proposed that this inhibitory effect of bile acid is mediated through inhibition of CCK-PZ secretion by high intraluminal concentrations of bile acid. Inhibition of CCK-PZ secretion by bile acid may contribute to the regulation of pancreatic and gallbladder function during digestion by reducing pancreatic enzyme secretion and permitting the gallbladder to refill after evacuation of its contents.

Adult↗

PubMed1989

Postprandial gallbladder motility during long term treatment with the long-acting somatostatin analog SMS 201-995 in acromegaly.

The effects on gallbladder motility of long term treatment with the somatostatin analog SMS 201-995 (SMS) were studied in five patients with acromegaly treated for 6-32 months with 200-300 micrograms SMS daily. SMS (100 micrograms) or placebo was injected sc 45 min before a standard breakfast. Gallbladder volume (ultrasonography), plasma cholecystokinin (CCK), and pancreatic polypeptide (PP) were measured until 120 min after the meal. SMS completely suppressed the postprandial gallbladder contraction, despite a blunted, though still statistically significant, increase in plasma CCK from 1.6 +/- 0.2 pmol/L to an average of 3.7 +/- 1.7 pmol/L (P less than 0.01). The postprandial plasma PP peak after placebo was replaced by a slight but statistically significant decrease after SMS (P less than 0.05). A statistically significant correlation between the plasma CCK values and corresponding gallbladder volumes was seen only after placebo injection, not in the SMS study. We conclude that during long term treatment of acromegalics with SMS, an injection of 100 micrograms, sc, completely abolishes gallbladder contraction for at least 2 h after a standard breakfast, despite blunted, but still significant, CCK release. The data suggest a decreased sensitivity of the gallbladder to endogenous CCK during long term treatment with SMS. Careful control of patients with respect to the formation of gallstones is recommended.

Acromegaly↗

PubMed2004

Jaundice predicts advanced disease and early mortality in patients with gallbladder cancer.

BACKGROUND: In patients with gallbladder cancer, jaundice suggests tumor involvement of the porta hepatis. This study reports on the prevalence, etiology, and clinical significance of jaundice in patients with gallbladder cancer. METHODS: Patients who presented with gallbladder cancer from 1995 to 2002 were entered into a prospective database. Disease-specific survival and clinicopathologic correlates were analyzed. RESULTS: Eighty-two (34%) of 240 patients with gallbladder cancer presented with jaundice. Jaundiced patients (96%) were more likely (P <.001) to have advanced-stage disease than nonjaundiced patients (60%). Only six (7%) jaundiced patients were resected with curative intent, and only four (5%) had negative surgical margins. This was significantly different from the nonjaundiced group, in which 62 patients (39%) had negative margins (P <.001). The median disease-specific survival in patients presenting with jaundice was 6 months and was significantly lower compared with 16 months in patients without jaundice (P <.0001). In the group presenting with jaundice, there were no disease-free survivors at 2 years, compared with 21% in the group without jaundice. CONCLUSIONS: Jaundice is common (34%) in patients who present with gallbladder cancer and is an indicator of advanced malignancy. These data do not support routine operative exploration of patients with jaundice secondary to gallbladder cancer.

Adult↗

PubMed1980

Effects of timepidium bromide, hyoscine-N-butylbromide and atropine on the isolated guinea pig gallbladder and sphincter of Oddi.

Effects of timepidium bromide (TB), hyoscine-N-butylbromide (HB) and atropine (Atr) were studied on the isolated guinea pig gallbladder and sphincter of Oddi. In the isolated gallbladder, the contraction induced by methacholine was competitively antagonized with TB, HB and Atr: pA2 values for TB, HB and Atr were 8.44, 7.55 and 9.11, respectively. Contraction of gallbladder after field stimulation at 5 Hz was also inhibited by TB, HB and Atr as well as by tetrodotoxin (TTX). On the other hand, TB had no significant influence on the electrically evoked (30 Hz) contraction which remained after treatment with TTX. It was estimated that the inhibitory activity of TB on the contraction of gallbladder was 1/5-1/6 that of Atr and 7 times as potent as HB. In the isolated sphincter of Oddi, TB, HB and Atr reduced the perfusion pressure increased by acetylcholine (ACh), the activity of TB being 1/4 that of Atr and 3 times of HB. The contractile responses to field stimulation (5 Hz) were also inhibited by TB, HB and Atr. The inhibitory activity of TB was 1/5 that of Atr and 12 times of HB. It was also demonstrated that TB produced no significant effect on the noradrenaline (Nor)-induced contraction and isoproterenol (Iso)-induced relaxation in the gallbladder or Nor-induced increase of the perfusion pressure in the sphincter of Oddi. It is suggested that TB acts on the gallbladder and sphincter of Oddi by virtue of its anticholinergic activity.

Acetylcholine↗

PubMed2001

Acidosis inhibits gallbladder contraction mediated by protein kinase C activation.

The effects of extracellular acidosis on gallbladder contraction were investigated using gallbladder strips isolated from guinea pigs. In an acidic medium (pH 6.9), gallbladder contraction induced by histamine and prostaglandin E2 was significantly lower than that in a normal medium (pH 7.4). Acidosis affected neither gallbladder contraction induced by histamine in the absence of extracellular Ca2+ nor that induced by KCl. Acidosis significantly inhibited Ca2+-induced contraction in the presence of sodium fluoride and phorbol 12,13-dibutyrate but not that in the presence of KCl. Staurosporine (30 nM) significantly inhibited gallbladder contraction induced by histamine and prostaglandin E2, but not that by KCl. Histamine-induced contraction in the presence of staurosporine was not affected by acidosis. Acidosis significantly inhibited Ca2+-induced contraction in the presence of histamine but not that in the presence of both histamine and staurosporine. These results suggest that extracellular acidosis selectively inhibits gallbladder contraction mediated by protein kinase C activation.

Acidosis↗

PubMed2006

The role of nitric oxide in the electrical field stimulation-induced contractions of sphincter of oddi and gallbladder strips in Guinea pigs.

The aim of this study was to investigate the modulatory role of nitric oxide (NO) in the electrical field stimulation (EFS)-induced contractions of isolated sphincter of Oddi (SO) and gallbladder strips from guinea pigs. EFS was used to activate the intrinsic nerves in SO and gallbladder strips. EFS produced frequency-dependent biphasic contractile responses in the SO strips. A smaller contraction, "on response", occurred during EFS, which was followed by a bigger contraction, "off response". Both responses were completely and irreversibly abolished by tetrodotoxin (TTX) (10(-6) M). Atropine (10(-6) M) inhibited the "on response", but not the "off response". EFS produced frequency-dependent monophasic contractile responses in gallbladder strips, which were completely and irreversibly abolished by TTX (10(-6) M) and atropine (10(-6) M). A nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine (10(-4) M and 3 x 10(-4) M, in SO and gallbladder strips, respectively), significantly increased all EFS-induced contractions of SO and gallbladder strips. L-Arginine, but not D-arginine reversed the effect induced by the NOS inhibitor, at all frequencies, in both strips. These results suggested that NO released from nitrergic nerve endings might play a regulatory role in the cholinergic neurotransmission of guinea pig SO and gallbladder strips. The "off response" in he SO preparations might be a rebound increase that was modulated by the nonadrenergic, noncholinergic inhibitory mediator NO.

Animals↗

PubMed2004

Compounded versus proprietary sincalide for evaluation of gallbladder ejection fraction.

OBJECTIVE: To report a comparison of compounded and proprietary sincalide in the evaluation of gallbladder ejection fraction during hepatobiliary scintigraphy. CASE SUMMARIES: Two patients were referred to nuclear medicine with symptoms consistent with hepatobiliary dysfunction. Both underwent hepatobiliary scintigraphy to evaluate anatomic and physiologic tract patency of the hepatobiliary system. Compounded sincalide, an adjuvant pharmaceutical used to evaluate gallbladder ejection fraction, was infused during hepatobiliary scintigraphy, and gallbladder ejection fractions were 11% and 24%, respectively. Hepatobiliary scintigraphy was repeated on both patients 72 hours later with proprietary sincalide used as the adjuvant pharmaceutical. The gallbladder ejection fractions were 32% and 72%, respectively. DISCUSSION: The use of sincalide to evaluate gallbladder ejection fraction in hepatobiliary scintigraphy is widely accepted in the surgical and nuclear medicine community. In late 2001, the sole manufacturer of sincalide announced indefinite unavailability of the product. Following the announcement, several compounding pharmacies began selling extemporaneously compounded sincalide as a replacement. Use of the compounded product has assumed therapeutic equivalence. CONCLUSIONS: Significant differences in gallbladder ejection fraction between compounded sincalide and sincalide in our patients are likely due to the intrinsic variability in response to sincalide. Clinicians should be aware of this variability, as well as the potential effect of concomitant medications.

Adult↗

PubMed1999

A study of the effect of benzylpenicillin on isolated human gallbladder.

The contractile effect of benzylpenicillin on isolated rings of human gallbladder was studied using preparations taken from surgical specimens after gallbladderectomy. The gallbladder was cut into two pieces and one ring was cut from each piece; one ring was mounted in a 100 ml organ bath containing Krebs solution and the isotonic changes of the preparation were recorded for each experiment. Benzylpenicillin (1 x 10(4) to 1 x 10(8) IU/l) was shown to exert a dose-dependent contractile effect on isolated human gallbladder rings which was blocked by atropine (1 x 10(-8) M). The benzylpenicillin-induced contractile effect was analogous to contraction observed with acetylcholine (1 x 10(-7) to 1 x 10(-2) M). The effect of benzylpenicillin on isolated human gallbladder may reflect a possible decrease in gallbladder emptying time in vivo, suggesting a beneficial effect of benzylpenicillin in antimicrobial treatment of gallbladder infections.

Acetylcholine↗

PubMed2025

A genome-wide screen in ex vivo gallbladders identifies Listeria monocytogenes factors required for virulence in vivo.

Listeria monocytogenes is a Gram-positive pathogen that causes the severe foodborne disease listeriosis. Following oral infection of the host, L. monocytogenes disseminates from the gastrointestinal tract to peripheral organs, including the gallbladder, where it replicates to high densities, establishing the gallbladder as the primary bacterial reservoir. Despite its importance in pathogenesis, little is known about how L. monocytogenes survives and replicates in the gallbladder. In this study, we assessed the L. monocytogenes genes required for growth and survival in ex vivo non-human primate gallbladders using a transposon sequencing approach. The screen identified 43 genes required for replication in the gallbladder, some of which were known to be important for virulence, and others had not been previously studied in the context of infection. We evaluated the roles of 19 genes identified in our screen both in vitro and in vivo, and demonstrate that most were required for replication in bile in vitro, for intracellular infection of murine cells in tissue culture, and for virulence in an oral murine model of listeriosis. Interestingly, strains lacking the mannose and glucose phosphoenolpyruvate-dependent phosphotransferase system (PTS) permeases Mpt and Mpo exhibited no defects in intracellular growth or intercellular spread, but were significantly attenuated during murine infection. While the roles of PTS systems in vivo were not previously appreciated, these results suggest that PTS permeases are necessary for extracellular replication during infection. Overall, this study demonstrates that L. monocytogenes genes required for replication in the gallbladder also play broader roles in disease.

Listeria monocytogenes↗

PubMed2002

Gallbladder management in obesity surgery.

BACKGROUND: In the 1980s, some surgeons recommended routine cholecystectomy for patients undergoing bariatric surgery. This was based on the high prevalence of gallstones in the obese and concern that rapid weight loss would increase the risk of gallbladder disease. Others recommended waiting for a lower weight and a definite need. With increasing prevalence and severity of obesity and increased use of gastric reduction surgery for weight control, it seemed appropriate to review the current standard of care for cholecystectomy. A survey was also made of ursodeoxycholic acid usage for prevention of gallstone formation. METHODS: Data collected from active contributors for the 28th Report of the International Bariatric Surgery Registry (IBSR) were examined. Two questionnaires were also sent to members of the American Society for Bariatric Surgery (ASBS). The first (Q1) asked about the indications for cholecystectomy. The second (Q2) asked about ursodeoxycholic acid usage for prevention of gallstone formation during rapid weight loss following surgical treatment of obesity. RESULTS: There has been an increase in concurrent cholecystectomy during the last 15 years. Some of this is due to a shift from simple gastric restrictive operations to gastric bypass with gastric restriction. When the most extensive bypass of intestine is used, as in distal Roux-en-Y gastric bypass (RYGBP-X) or biliopancreatic diversion with a duodenal switch (BPD-DS), all patients were reported to have undergone cholecystectomy. Only 30% of surgeons performing standard Roux-en-Y gastric bypass (RYGBP) remove normal-appearing gallbladders. Ursodeoxycholic acid is used to prevent gallstone formation in one-third of patients when a normal-appearing gallbladder is left in place. CONCLUSIONS: Prophylactic cholecystectomy is left to the discretion of the surgeon when RYGBP is used. There has been an increase in cholecystectomy and malabsorptive operations during the last 15 years. When most of the small bowel is bypassed, all remaining gallbladders are removed. For patients with simple restriction operations, normal-appearing gallbladders are usually left in place. Urso-deoxycholic acid during rapid weight loss for prevention of gallstone formation is used in one-third of patients with remaining gallbladders.

Adult↗

PubMed2005

Gallbladder pathology in morbid obesity.

BACKGROUND: Obese patients are at increased risk for biliary disease. The prevalence and type of gallbladder pathology in morbidly obese patients was evaluated, and compared with a non-obese control group. METHODS: A consecutive series of obese patients (n=478) who had undergone bariatric surgery with concurrent routine cholecystectomy and a consecutive group of organ donors (n=481) were compared. Gallbladder pathology was defined as: cholelithiasis, cholecystitis, cholesterolosis, or normal pathology. RESULTS: Mean age of obese patients and of donors was 42 +/- 9 and 43 +/- 17 years respectively and mean BMI was 52 +/- 10 and 27 +/- 7 kg/m2 respectively, P<0.05. There were more females in the obesity group (88% vs 47%, P<0.0001). 31% of obese patients and 7% of controls had a previous cholecystectomy (P<0.0001). 21% of the obese and 72% of the controls had normal gallbladder pathology (P<0.0001). Overall, obese patients had a higher incidence of cholelithiasis (25% vs 5%, P<0.0001), cholecystitis (50% vs 17%, P<0.0001), and cholesterolosis (38% vs 6%, P<0.0001) compared with controls. Obese patients with BMI <50 were more likely than those with BMI > or =50 to have normal gallbladder pathology (27% vs 14%, P<0.001). Female patients were more likely to have undergone previous cholecystectomy than males in both the obese group (34% vs 11%, P<0.001) and the control group (12% vs 2%, P<0.0001). Normal pathology was more common in male patients (80% vs 63%, P<0.0001) and patients <50 years (76% vs 66%, P<0.05) in the control group. CONCLUSIONS: Obese patients have an increased incidence of benign gallbladder disease than a group of controls, and the relative risk appears to be positively correlated with the level of increase in the BMI. Obesity appears to change the effect of age and gender on gallbladder pathology.

Adolescent↗

PubMed2000

Delay in gallbladder emptying during the perimenopausal period.

A pilot study has ascribed an important role in gallbladder motility and emptying to the perimenopausal period. To assess the effect of this period on gallbladder emptying and cholelithogenesis, 25 women in the perimenopausal period without gallbladder disease were submitted to cholangiography and two ultrasound exams. The time for gallbladder emptying and the presence of cholelithiasis were assessed. All patients presented a delay in gallbladder emptying with no relationship to the pre- or postmenopausal period. This finding was not related to lithogenesis. Gallbladder emptying time is longer during the perimenopausal period.

Adult↗

PubMedDate not supplied

Relationship between cholecystolithiasis and polypoid gallbladder.

OBJECTIVE: To study the relationship between cholecystolithiasis and polypoid gallbladder (PLG), 260 patients with polypoid gallbladder were investigated. The patients were divided into 2 groups: group A (PLG combined with cholecystolithiasis) and group B (without cholecystolithiasis). The clinical pathological characteristics were analyzed. The intestinal epithelium metaplasia and atypical hyperplasia of the gallbladder mucosa were observed under light microscope. RESULTS: Intestinal epithelium metaplasia and atypical hyperplasia of gallbladder mucosa were found in 47 of the 260 cases. The pathological lesions included 16 gallbladder carcinoma, 11 adenomatosis polyp, 5 myoadenoma, 7 cholesterol polyp, 4 inflammatory polyp and 4 adenomatosis hyperplasia, which occurred in 26 and 21 patients in group A and group B, i.e. 44.0% and 10.3% respectively. The difference between group A and group B was statistically significant (P<0.01). CONCLUSION: Cholecystolithiasis and the succeeding inflammatory reaction is a risk-factor for the polypoid gallbladder to develop tumour.

Adolescent↗

PubMed2002

Anatomical and neuropeptidergic properties of the duodenal neurons projecting to the gallbladder in the golden hamster.

This study investigated the anatomical and neuropeptidergic properties of the duodenal neurons projecting to the gallbladder in the golden hamster. Fast blue (FB) was injected into the subserosa of the gallbladder in order to identify by retrograde tracing the duodenal neurons that project to the gallbladder. Subsequently, immunofluorescence microscopy was employed to see whether these duodenal neurons contained putative peptidergic neurotransmitters such as calcitonin gene-related peptide (CGRP), galanin (GAL) and vasoactive intestinal polypeptide (VIP). The FB-labeled cells were only found in the duodenal region adjacent to the major duodenal papilla where the biliary duct opens. On the other hand, there was no difference within this duodenal region in the numbers of FB-labeled cells between the mesenteric and antimesenteric portions, suggesting that these two portions of the duodenum equally contribute neuronal projections to the gallbladder. Double-immunofluorescence microscopy clearly demonstrated that a small population of FB-positive duodenal neurons contained putative neurotransmitters CGRP, GAL and VIP. Our data suggest that duodenal neurons around the major duodenal papilla in the golden hamster project to the gallbladder and exert their influence on the gallbladder via neuropeptides such as CGRP, GAL and VIP.

Animals↗

PubMed2006

Cyclooxygenase-2 expression determines neo-angiogenesis in gallbladder carcinomas.

Neo-angiogenesis may have an important role in the poor prognosis of gallbladder carcinoma. An enhanced expression of COX-2 was found in precancerous lesions and in gallbladder carcinoma, likely to be involved in carcinogenesis as well as in angiogenesis. To study the relationships between the COX-2 expression and degree of vascularization, as well as to evaluate their role in the prognosis of patients with gallbladder carcinoma. 27 cases of gallbladder adenocarcinoma were included, classified grading I-III according the WHO classification. The COX-2 and endothelial antigen CD105 expressions were assessed immunohistochemically. COX-2 expression was evaluated according to the percentage and staining intensity of positive cells into "COX-2 positive" and "COX-2 negative" groups. In order to assess tumor microvessel density (MVD), CD105 positively stained microvessels were counted for each specimen in predominantly vascular areas (hot spots) at 200 x magnification. The MVD ranged from 9 to 46 microvessels/field. 15 tumors belonged to the hypervascular group (MVD > or = 25) and 12 to the hypovascular group. There were 16 (59.2%) COX-2 positive cases. There was difference in the degree of angiogenesis between COX-2 positive vs. COX-2 negative group: 11 (68.8%) out of 16 "COX-2 positive" tumors were hypervascular, in comparison with just 4 (36.4%) of "COX-2 negative" tumors. Our data show that the MVD corresponds to the COX-2 overexpression in gallbladder carcinomas. Augmented tumor neovascularization induced by COX-2 might be responsible for the poor prognosis in gallbladder carcinoma patients.

Adenocarcinoma↗