Canine Gallbladder Research Articles

Comprehensive gene expression analysis in gallbladder mucosal epithelial cells of dogs with gallbladder mucocele.

Gallbladder mucocele (GBM) is a common disease in the canine gallbladder. Although the pathogenesis of GBM remains unclear, we recently reported that the excessive accumulation of mucin in the gallbladder is not a result of overproduction by gallbladder epithelial cells (GBECs). Changes in the function of GBECs other than the production of mucin are associated with the pathogenesis of GBM. We performed an RNA sequencing (RNA-seq) analysis to comprehensively search for abnormalities in gene expression profiles of GBECs in dogs with GBM. Fifteen dogs with GBM and 8 dogs euthanized for reasons other than gallbladder disease were included. The GBECs were isolated from gallbladder tissues to extract RNA. The RNA-seq analysis was performed using the samples from 3 GBM cases and 3 dogs with normal gallbladders, and the gene expression profiles were compared between the 2 groups. Differences in mRNA expression levels of the extracted differentially expressed genes (DEGs) were validated by quantitative reverse transcription polymerase chain reaction (RT-qPCR) using samples of 15 GBM cases and 8 dogs with normal gallbladders. Comparison of gene expression profiles by RNA-seq extracted 367 DEGs, including ANO1, a chloride channel associated with changes in mucin morphology, and HTR4, which regulates the function of chloride channels. The ANO1 and HTR4 genes were confirmed to be downregulated in the GBM group by RT-qPCR. Our results suggest that GBM may be associated with decreased function of chloride channels expressed in GBECs.

Acquired dysfunction of CFTR underlies cystic fibrosis-like disease of the canine gallbladder.

Mucocele formation in dogs is a unique and enigmatic muco-obstructive disease of the gallbladder caused by the amassment of abnormal mucus that bears striking pathological similarity to cystic fibrosis. We investigated the role of cystic fibrosis transmembrane conductance regulatory protein (CFTR) in the pathogenesis of this disease. The location and frequency of disease-associated variants in the coding region of CFTR were compared using whole genome sequence data from 2,642 dogs representing breeds at low-risk, high-risk, or with confirmed disease. Expression, localization, and ion transport activity of CFTR were quantified in control and mucocele gallbladders by NanoString, Western blotting, immunofluorescence imaging, and studies in Ussing chambers. Our results establish a significant loss of CFTR-dependent anion secretion by mucocele gallbladder mucosa. A significantly lower quantity of CFTR protein was demonstrated relative to E-cadherin in mucocele compared with control gallbladder mucosa. Immunofluorescence identified CFTR along the apical membrane of epithelial cells in control gallbladders but not in mucocele gallbladder epithelium. Decreases in mRNA copy number for CFTR were accompanied by decreases in mRNA for the Cl-/[Formula: see text] exchanger SLC26A3, K+ channels (KCNQ1, KCNN4), and vasoactive intestinal polypeptide receptor (VIPR1), which suggest a driving force for change in secretory function of gallbladder epithelial cells in the pathogenesis of mucocele formation. There were no significant differences in CFTR gene variant frequency, type, or predicted impact comparing low-risk, high-risk, and definitively diagnosed groups of dogs. This study describes a unique, naturally occurring muco-obstructive disease of the canine gallbladder, with uncanny similarity to cystic fibrosis, and driven by the underlying failure of CFTR function.NEW & NOTEWORTHY Cystic fibrosis transmembrane conductance regulatory protein (CFTR) genomic variants and expression of mRNA, protein, and electrogenic anion secretory activity of CFTR were characterized in dog gallbladder. Acquired inhibition of CFTR expression by gallbladder epithelium was identified as underpinning a naturally occurring muco-obstructive disease of the dog gallbladder that bears striking pathological similarity to animal models of cystic fibrosis.

Canine Gallbladder Erosion/Ulcer and Hemocholecyst: Clinicopathological Characteristics of 14 Cases.

(1) Background: Gallbladder mucosal erosion and/or ulceration are illnesses associated with unexpected gallbladder intra-cystic bleeding (hemocholecyst), an under-reported problem in dogs. (2) Methods: Clinicopathological characteristics of 14 dogs with gallbladder erosion/ulcer were investigated in this single-center retrospective study using clinical data and archived gallbladder tissues of client-owned dogs. (3) Results: Canine gallbladder erosion/ulcer tends to occur in older, neutered dogs of various breeds. Vomiting, lethargy, and anorexia are common. Concurrent gallbladder rupture occurred in 5/14 cases (35.7%), while rupture was absent in 6/14 cases (42.8%) and undetermined in 3/14 (21.4%) cases. Histologically, the gallbladder wall was markedly thickened due to mucosal hyperplasia, inflammatory infiltrates, fibrosis, edema, hemorrhage, and smooth muscle hyperplasia/hypertrophy. Twelve out of fourteen cases (85.7%) had concurrent cholecystitis of varying severity. Bacteria were detected by Giemsa or Warthin-Starry stain in 8/14 (57.1%) cases. Bacterial rods immunoreactive to the anti-Helicobacter antibody were present in one case. Mucosal epithelial cells of the gallbladder erosion/ulcer cohort were immunopositive for the cyclooxygenases COX-1 or COX-2 in only 5/14 (35.7%) cases. In contrast, COX-1 and COX-2 were more frequently expressed in a reference pool of cases of gallbladder mucocele (n = 5) and chronic cholecystitis (n = 5). COX-1 was expressed in 9/10 cases (90.0%) of gallbladder mucocele and chronic cholecystitis and in 10/10 cases (100%) for COX-2. (4) Conclusions: Canine gallbladder erosion/ulcer is an under-reported condition which requires active clinical intervention. Based on the clinicopathological information reported in this study in addition to the COX-1 and COX-2 IHC results, we suggest that canine gallbladder erosion/ulcer may be related to decreased cytoprotection physiologically provided by arachidonic acid, but which is decreased or absent due to reduced COX expression because of yet undetermined etiologies.

Increased radiographic opacity in the region of the gallbladder can be identified in dogs with large amounts of gallbladder sediment, sludge balls, and gallbladder mucocele.

Increased soft-tissue opacity in the region of the canine gallbladder is incidentally detected on radiographs. We hypothesized that there is a difference in the detection of gallbladder sediment on radiographs depending on the amount or mobility of the sediment. In this retrospective and analytical study, we aimed to assess the ultrasonographic features of gallbladder sediment that were detected radiographically. We also aimed to assess the differences in the detection of increased opacity of the gallbladder between radiographic views. We included 223 dogs that underwent thoracic radiography, abdominal radiography, and gallbladder ultrasonography. Ultrasonographic images of the gallbladder were divided into five groups: group 1, gravity-dependent sediment occupying<50% of the gallbladder; group 2, gravity-dependent sediment occupying ≥50%; group 3, sediment attached to the gallbladder wall; group 4, sludge ball; and group 5, gallbladder mucocele. Dogs showing increased opacity on subjective assessment of any radiographic view were recorded, and the sensitivity of radiographic views for detecting gallbladder sediment was analyzed. Of 168 dogs with gallbladder sediment, 37 had increased opacity on at least one radiographic projection. The frequency was compared as a percentage within each category, and Group 4 was the highest percentage with increased radiographic gallbladder opacity, followed by Groups 2 and 5. The sensitivity for detecting increased opacity was highest in the thoracic ventrodorsal view. Thus, in dogs with increased gallbladder opacity on radiographs, large amounts of gallbladder sediment, sludge balls, and gallbladder mucocele should be considered differential diagnoses. In addition, the thoracic ventrodorsal view is recommended to evaluate gallbladder opacity.

Ultrasonographic particularities of chronic gallbladder cholecystitis in dogs

Canine gallbladder related diseases are being reported with an increased frequency by specialists working in small animal veterinary medicine. It is presumed that these represent a direct consequence following changes in diet, lifestyle and activity levels of small animals. As a result of increased assertion towards the well-being of pets worldwide, veterinary medicine has evolved by creating and implementing new diagnostic protocols and noninvasive means of investigations, like ultrasonography, which can characterize the presence and intensity of any abnormalities encountered in the canine gallbladder.

MUC5AC and MUC5B expression in canine gallbladder mucocele epithelial cells.

Gallbladder mucocele (GBM) is one of the most common gallbladder diseases in dogs. Its pathogenesis has not yet been clarified, but excessive accumulation of a secretory gel-forming mucin, MUC5AC in the gallbladder has been reported. This study aimed to ascertain if MUC5AC overproduction resulted in mucus accumulation in the gallbladder during GBM development. Eleven dogs undergoing cholecystectomy who were pathologically diagnosed with GBM were included, and the expression level of mucins, particularly MUC5AC and MUC5B, in their gallbladder epithelial cells was compared with those in normal gallbladder epithelial cells. On reverse transcription-quantitative polymerase chain reaction screening, there was a significant difference (P<0.05) in the mRNA expression level of MUC1, but not of other mucins including MUC5AC and MUC5B, between mucocele and normal gallbladder epithelial cells. Protein expression levels were also evaluated for MUC5AC and MUC5B using immunohistochemistry. There was little immunoreactivity for MUC5AC, whereas MUC5B showed definitive staining in gallbladder epithelial cells. There was no difference in MUC5AC and MUC5B protein expression levels between mucocele and normal gallbladder epithelial cells. These data suggest that excessive production of mucin, especially MUC5AC and MUC5B, does not occur in canine GBM, and that abnormal mucus excretion, rather than excessive mucus production, may be the cause of GBM development.

CT findings of bleeding from a canine gall bladder carcinoid tumour

AbstractA 10‐year‐old, male Boston terrier was presented with chronic haematemesis and melena. On computed tomography, a mass arising from the gall bladder was observed to be homogeneous and strongly enhanced compared with surrounding liver in the arterial phase. The attenuation of lesion around the mass in the gall bladder showed 60 Hounsfield units and no contrast enhancement. Endoscopic examination revealed haemorrhage around the duodenal papilla. Surgery revealed that the gall bladder was filled with a blood clot originating from the mass. Histopathology of the mass in the gall bladder revealed it to be a carcinoid tumour. The dog survived and remained disease‐free for 45 months without adjuvant chemotherapy.

Screening of bacterial DNA in bile sampled from healthy dogs and dogs suffering from liver- or gallbladder-associated disease.

Although the biliary system is generally aseptic, gallbladder microbiota has been reported in humans and some animals apart from dogs. We screened and analyzed the bacterial deoxyribonucleic acid in canine gallbladders using bile sampled from 7 healthy dogs and 52 dogs with liver- or gallbladder-associated disease. PCR screening detected bacteria in 17.3% of diseased dogs (9/52) and none in healthy dogs. Microbiota analysis of PCR-positive samples showed that the microbial diversity differed between liver- and gallbladder-associated disease groups. Thus, a specific bacterial community appears to occur at a certain frequency in the bile of diseased dogs.

Chronic Cholecystitis of Dogs: Clinicopathologic Features and Relationship with Liver

Simple SummaryThis study on the gallbladders and livers of 219 client-owned dogs provides a benchmark for future studies on chronic canine cholecystitis. The statistical evaluation of clinical data; histopathology; histochemistry; and immunohistochemistry in this report provides insight into the etiology of chronic cholecystitis in dogs(1) Background: Chronic cholecystitis of dogs has not been vigorously investigated histopathologically. In addition, the relationship between gallbladder and liver diseases is not known. (2) Methods: We aimed to provide a hallmark for canine chronic cholecystitis using clinical data, histopathology, histochemistry, immunohistochemistry, and statistical analysis. (3) Results: Our investigation of 219 ultrasonographically abnormal surgically resected canine gallbladders revealed 189 cases (86.3%) of mucosal lymphoplasmacytic infiltration (chronic cholecystitis). Sludge, a gravity-dependent or nondependent fine granular hyperechoic material, was more prevalent (105/219, 47.9%) than mucocele (51/219, 23.2%) in this cohort. Mucosal lymphoid follicles were detected in 68/219 cases (31%), suggesting the influence of long-standing antigenic stimulation. Bacteria were histochemically detected in 41/60 (68.3%) of heavily inflamed gallbladders, 18/129 (14%) of lightly inflamed, and 3/18 (16.7%) of uninflamed gallbladders, suggesting a possible relationship between bacteria and chronic cholecystitis. Simultaneous liver biopsies revealed mild or no inflammation, changes consistent with primary portal vein hypoplasia, and mild hepatocellular degeneration. (4) Conclusions: Based on the results of our statistical analysis, we conclude that canine chronic cholecystitis is a long-standing inflammatory process of unknown (but possibly bacterial) etiology and that liver pathology is unlikely the cause of chronic cholecystitis in dogs.

CT attenuation values and mineral distribution can be used to differentiate dogs with and without gallbladder mucoceles.

Gallbladder mucoceles are potentially fatal in dogs. Multiphase CT angiography was performed to evaluate the canine gallbladder in three conditions: no sludge, sludge occupying ≥25% of the lumen, and mucoceles. Twenty dogs with normal hepatobiliary bloodwork and no-to-minimal gallbladder sludge, 13 dogs with normal bloodwork and ≥25% sludge in the gallbladder lumen, and 18 dogs with histologically confirmed gallbladder mucoceles were enrolled in a prospective, observational diagnostic accuracy study. Three regions of interest (ROI) were stratified in the dorsal-ventral orientation and a single ROI was measured within the hepatic parenchyma. Mean attenuation and presence of mineral were recorded. Average Hounsfield units (HU) were recorded for precontrast, arterial, portovenous, and late venous phases. The overall median HU value for mucoceles was significantly higher than gallbladders without sludge and with sludge; precontrast median overall attenuation was 49.3, 35.8, and 39.7 HU, respectively (P<.000004). Mineral was seen in four (20%) dogs with no sludge, seven (56%) dogs with sludge, and nine (50%) dogs with mucoceles. Mineral in the dogs with mucoceles was located within the central aspect of the gallbladder lumen in 67% of mucoceles; this mineral distribution was not seen in any dog without a mucocele. Computed tomography can differentiate a subset of gallbladder mucoceles from dogs with and without gallbladder sludge, especially in the precontrast series. An HU value of 48.6 is 52% sensitive and 96% specific for a gallbladder mucocele. A hyperattenuating gallbladder on precontrast CT images and centrally distributed mineral can be a gallbladder mucocele.

Changes in pre- and postoperative serum leptin concentrations in dogs with gallbladder mucocele and cholelithiasis

BackgroundLeptin has been shown to have various physiological and pathological roles in the canine gallbladder. In this study, we performed pre- and postoperative short-term follow-up analyses to confirm changes in serum leptin levels before and after cholecystectomy due to gallbladder mucocele (GBM) or cholelithiasis in dogs.ResultsTwenty-six cholecystectomized dogs (GBM: n = 14; cholelithiasis: n = 12) for prophylactic or clinical symptom relief were enrolled in the present study. Dogs were subgrouped according to clinical symptoms and prognosis after surgery as follows: 1) asymptomatic group (n = 13), 2) recovery group (n = 8), and 3) death group (n = 5). Liver enzymes, total bilirubin, lipid profiles, and leptin concentrations were determined from sera on the pre-operative day and at 1, 3, and 7 days postoperation. Serum leptin concentrations were gradually but significantly decreased in the asymptomatic group (p = 0.008, 0.004, and 0.004 on days 1, 3, and 7, respectively, compared with that before surgery) and the recovery group (p = 0.048 and 0.048 on days 3 and 7, respectively, compared with that before surgery). However, in the death group, leptin concentrations did not differ significantly over time (p = 0.564). Additionally, serum leptin levels in the recovery group (p = 0.006) and death group (p = 0.021) were significantly higher than those in the asymptomatic group. Liver enzymes and total bilirubin (T-Bil) were significantly decreased only in the recovery group, particularly on day 7. In the asymptomatic group, liver enzymes and T-Bil were not changed significantly over time, and in the death group, only T-Bil was significantly decreased on day 7. Total cholesterol and triglyceride levels were not significantly decreased over time in all groups.ConclusionsThese results indicate that leptin is a potential biomarker reflecting the severity and prognosis of GBM and cholelithiasis both before and after cholecystectomy in dogs.

Pancreatic Choristoma in a Canine Gallbladder

A 1.5-year-old male Siberian Husky dog was presented with a history of progressive twitching and tetraplegia. The dog was humanely destroyed and at necropsy examination an incidental intramural white lesion measuring 10×15×5mm was observed in the gallbladder. Histologically, the mass consisted of pancreatic tissue located in the tunica adventitia of the gallbladder. Immunohistochemistry revealed that the islets of Langerhans were positive for insulin, but negative for glucagon. In addition, the dog had non-suppurative meningoencephalitis associated with canine distemper virus infection. The gallbladder lesion was consistent with pancreatic choristoma and is the first case described in a canine gallbladder.

Associations between serum leptin levels, hyperlipidemia, and cholelithiasis in dogs.

Leptin and its receptor play several physiological roles in the canine gallbladder, and the dysregulation of leptin might play a role in the pathogenesis of gallbladder diseases such as gallbladder mucocele. Previous studies revealed a positive association between hyperlipidemia and gallstones in humans. However, the latter is still unclear in dogs with cholelithiasis. In this study, we examined the differences in leptin, leptin receptor, total cholesterol, and triglyceride levels between healthy dogs and dogs with cholelithiasis, and evaluated the correlation between leptin and hyperlipidemia. Twenty-eight healthy dogs and 34 client-owned dogs with cholelithiasis were enrolled in the study. Leptin concentrations and lipid profiles were determined from sera, and leptin and leptin receptor expression levels were quantified in gallbladder tissue. In dogs with cholelithiasis, serum concentrations of leptin (p < 0.001), total cholesterol (p < 0.001), and triglycerides (p < 0.001) were significantly higher compared with those in healthy dogs. Positive correlations were observed between serum leptin and total cholesterol (95% confidence interval (CI) = 0.61–0.89, r = 0.725, p < 0.001), and between leptin and triglycerides (95% CI = 0.63–0.89, r = 0.782, p < 0.001) in the cholelithiasis group. Hypercholesterolemia (Odds Ratio (OR) = 9.720; 95% CI = 1.148–82.318) and hypertriglyceridemia (OR = 12.913; 95% CI = 1.548–107.722) were shown to be risk factors for gallstone disease. In cholelithiasis patients who underwent cholecystectomy, serum leptin levels were significantly higher than in patients that had not undergone surgery (p < 0.001). Leptin and leptin receptor expression was upregulated in the gallbladder tissues of cholelithiasis patients (p < 0.01 and p < 0.001, respectively). These results indicate that increased serum leptin concentrations and hyperlipidemia (hypercholesterolemia or hypertriglyceridemia) are associated with canine cholelithiasis and that homeostatic imbalance of these parameters might affect the pathogenesis of gallstones.

Increased Leptin and Leptin Receptor Expression in Dogs With Gallbladder Mucocele.

BackgroundLeptin and its receptor play a role in several disease processes such as pancreatitis and heart disease. However, their association with gallbladder mucocele (GBM) in dogs has not been reported.Hypothesis/ObjectivesTo evaluate differences in the expression of leptin and leptin receptor between dogs with and without GBM.AnimalsTwenty‐five healthy dogs, including 9 laboratory beagle dogs, and 22 client‐owned dogs with GBM.MethodsSerum leptin concentration was determined in blood samples of all dogs by ELISA. Canine gallbladder samples were collected from 9 dogs with GBM that underwent surgery for therapeutic purposes and from 9 healthy laboratory beagle dogs as a normal control group. Samples were analyzed for leptin and leptin receptor mRNA by real‐time polymerase chain reaction.ResultsSerum leptin concentration was significantly higher in dogs with GBM than in healthy dogs (medians of 7.03 and 2.18 ng/mL, respectively; P < .001). Patients with GBM that had undergone surgery had significantly higher serum leptin concentrations than those that had not (medians of 12.2 and 4.09 ng/mL, respectively; P = .001). However, no difference in serum leptin concentration was found between dogs with GBM with or without endocrinopathies. The mRNA expression levels of leptin and its receptor were significantly increased in the gallbladder tissues of dogs with GBM.Conclusions and Clinical ImportanceDysregulation of leptin might be involved in the pathophysiology of GBM, and leptin concentrations might be associated with GBM severity.

Retrospective analysis of canine gallbladder contents in biliary sludge and gallbladder mucoceles.

The pathophysiology of canine gallbladder diseases, including biliary sludge, gallbladder mucoceles and gallstones, is poorly understood. This study aimed to evaluate the component of gallbladder contents and bacterial infection of the gallbladder in order to elucidate the pathophysiology of biliary sludge and gallbladder mucoceles. A total of 43 samples of canine gallbladder contents (biliary sludge, 21 and gallbladder mucoceles, 22) were subjected to component analysis by infrared spectroscopy, and the resultant infrared spectra were compared with that of swine mucin. Of the 43 samples, 41 were also evaluated by aerobic and anaerobic bacterial culture. The contents of 20 (95.2%) biliary sludge and 22 (100%) gallbladder mucocele samples exhibited similar infrared spectra as swine mucin. Although biliary sludge and gallbladder mucocele contents exhibited similar infrared spectra, one sample of biliary sludge (4.8%) was determined to be composed of proteins. The rate of bacterial infection of the gallbladder was 10.0% for biliary sludge and 14.3% for gallbladder mucoceles. Almost all of the identified bacterial species were intestinal flora. These results indicate that the principal components of gallbladder contents in both gallbladder mucoceles and biliary sludge are mucins and that both pathophysiologies exhibit low rates of bacterial infection of the gallbladder. Therefore, it is possible that gallbladder mucoceles and biliary sludge have the same pathophysiology, and, rather than being independent diseases, they could possibly represent a continuous disease. Thus, biliary sludge could be considered as the stage preceding the appearance of gallbladder mucoceles.

Presence and distribution of leptin and leptin receptor in the canine gallbladder

The hormone leptin is produced by mature adipocytes and plays an important role in regulating food intake and energy metabolism through its interaction with the leptin receptor. In addition to roles in obesity and obesity-related diseases, leptin has been reported to affect the components and secretion of bile in leptin-deficient mice. Furthermore, gallbladder diseases such as cholelithiasis are known to be associated with serum leptin concentrations in humans. We hypothesized that the canine gallbladder is a source of leptin and that the leptin receptor may be localized in the gallbladder, where it plays a role in regulating the function of this organ. The aim of this study was to demonstrate the presence and expression patterns of leptin and its receptors in normal canine gallbladders using reverse transcriptase-PCR (RT-PCR) and immunohistochemistry. Clinically normal gallbladder tissue samples were obtained from four healthy beagle dogs with similar body condition scores. RT-PCR and sequencing of the amplified PCR products revealed the presence of leptin mRNA and its receptors in the gallbladder. Immunohistochemical investigations demonstrated the expression of leptin and its receptors in the luminal single columnar and tubuloalveolar glandular epithelial cells. In conclusion, the results of this study demonstrated the presence of leptin and its receptors in the gallbladders of dogs. Leptin and its receptor were both localized throughout the cytoplasm of luminal and glandular epithelial cells. These results suggested that the gallbladder is not only a source of leptin, but also a target of leptin though autocrine/paracrine mechanisms. The results of this study could increase the understanding of both the normal physiological functions of the gallbladder and the pathophysiological mechanisms of gallbladder diseases characterized by leptin system dysfunction.

Lack of association of ABCB4 insertion mutation with gallbladder mucoceles in dogs.

The etiology of canine gallbladder mucocele (GBM) has not yet been identified. However, several studies have linked GBM in dogs to particular breeds (Shetland Sheepdogs are commonly implicated), concurrent endocrine disease (hyperadrenocorticism and/or hypothyroidism), and a mutation in the canine ABCB4 gene (ABCB4 1583_1584G), particularly in Shetland Sheepdogs. The current study assessed ABCB4 1583_1584G, in a wider sample of dogs with GBM compared with age and breed-matched controls. ABCB4 1583_1584G was identified in 4 of 8 Shetland Sheepdogs and 13 of 28 other breeds with GBM. ABCB4 1583_1584G was also detected in 9 of 12 Shetland Sheepdogs and 23 of 37 other breeds that did not have GBM. No statistically significant association existed between ABCB4 1583_1584G and the presence of GBM for all dogs combined or for Shetland Sheepdogs alone. In contrast to previously reported findings, the current study did not identify a strong association between ABCB4 1583_1584G and GBM in Shetland Sheepdogs or other breeds.

PHYSIOLOGIC VARIANTS, BENIGN PROCESSES, AND ARTIFACTS FROM 106 CANINE AND FELINE FDG‐PET/COMPUTED TOMOGRAPHY SCANS

18F-Fluoro-deoxyglucose positron emission computed tomography (FDG-PET/CT) is an emerging diagnostic imaging modality in veterinary medicine; however, little published information is available on physiologic variants, benign processes, and artifacts. The purpose of this retrospective study was to describe the number of occurrences of non-neoplastic disease-related FDG-PET/CT lesions in a group of dogs and cats. Archived FDG-PET/CT scans were retrieved and interpreted based on a consensus opinion of two board-certified veterinary radiologists. Non-neoplastic disease-related lesions were categorized as physiologic variant, benign activity, or equipment/technology related artifact. If the exact cause of hypermetabolic areas could not be determined, lesions were put into an indeterminate category. A total of 106 canine and feline FDG-PET/CT scans were included in the study. In 104 of the 106 scans, a total of 718 occurrences of physiologic variant, areas of incidental benign activity, and artifacts were identified. Twenty-two of 23 feline scans and 82 of 83 canine scans had at least one artifact. Previously unreported areas of increased radiopharmaceutical uptake included foci associated with the canine gall bladder, linear uptake along the canine mandible, and focal uptake in the gastrointestinal tract. Benign activity was often seen and related to healing, inflammation, and indwelling implants. Artifacts were most often related to injection or misregistration. Further experience in recognizing the common veterinary FDG physiologic variation, incidental radiopharmaceutical uptake, and artifacts is important to avoid misinterpretation and false-positive diagnoses.

In-vitro Effect of Pirenzepine on Motility of Canine Gall-bladder

The action of pirenzepine as an antimuscarinic drug has been investigated on motor responses of muscle strips in the canine gall-bladder. Pirenzepine was further used to examine whether gall-bladder motor responses to synthetic sulphated cholecystokinin octapeptide (CCK-8) are sensitive to pirenzepine. Pirenzepine (10(-9)-10(-5) M) antagonized muscle contractions in response to acetylcholine (10(-9)-10(-2) M) and CCK-8 (10(-11)-10(-6) M) in a significant manner. These findings indicate that pirenzepine is a potent antagonist of two substances that are the principal contractile mediators of gall-bladder contraction and suggest that long-term administration of pirenzepine could contribute to stasis of the gall-bladder.

M1001 The Effects of HMG-CoA Reductase Inhibitors (Statins) on Expression of COX-2 in Cultured Canine Gallbladder Epithelial Cells

M1001 The Effects of HMG-CoA Reductase Inhibitors (Statins) on Expression of COX-2 in Cultured Canine Gallbladder Epithelial Cells