Dispositions of caffeine and antipyrine were compared as indicators of decreasing hepatic function in dogs with experimentally induced progressive liver disease. Dimethylnitrosamine, a hepatospecific toxin, was administered orally to 16 dogs; 6 dogs served as controls (group 1). Three classes of liver disease were defined by histologic features: mild (group 2; n = 5), moderate (group 3; n = 6), and severe (group 4; n = 5). Disposition of antipyrine, and 24 hours later, caffeine was studied 3 weeks after the last dose of toxin in each dog. For both drugs, rapid IV administration of 20 mg/kg of body weight was administered and serum samples were obtained at intervals for determination of at least 5 terminal-phase drug half-lives. For both drugs, clearance and mean residence time differed among groups (P less than or equal to 0.01). Clearance of antipyrine and caffeine was decreased in groups 3 and 4, compared with groups 1 and 2. Antipyrine and caffeine mean residence times were longer in group-3 dogs, compared with dogs of groups 1 and 2. Correction of caffeine and antipyrine clearances for hepatic weight increased discrimination between groups 3 and 4. The clearance and mean residence time ratios of antipyrine to caffeine were calculated for each group and, when compared with values for group-1 dogs, were used to test for differences between the 2 drugs in response to disease. Ratios did not differ among groups. These results indicate that the disposition of antipyrine and caffeine may change similarly with progression of dimethylnitrosamine-induced liver disease.

Disposition kinetics of indocyanine green (ICG) were used to evaluate hepatic function in healthy Beagles (group 1; n = 6) and Beagles with progressive hepatic disease induced by oral administration of dimethylnitrosamine, a hepatospecific toxin. Three classes of hepatic disease were defined by histologic features: mild (group 2; n = 5), moderate (group 3; n = 6), and severe (group 4; n = 5). Disposition of ICG was studied 3 weeks following the last dose of toxin. A rapid IV injection of 0.5 mg of ICG/kg was administered and serum samples were obtained at certain intervals during 60-minute periods. Serum ICG was analyzed by use of visible spectrophotometry. Disposition kinetics were determined from serum ICG concentrations vs 15- and 60-minute time curves and compared between one another and among groups. Data based on 60-minute time curves were not significantly different from those based on 15-minute curves. Area under the curve for ICG was greatest in group 3. Clearance of ICG was decreased and mean resident time was increased in groups 3 and 4, compared with those in groups 1 and 2. When disposition data (60 minutes) were normalized for differences in hepatic weight among dogs, group-3 mean resident time was significantly greater than that of group 4. This study supports the diagnostic benefits of using ICG disposition kinetics as a method of evaluating hepatic function in dogs with progressive liver disease.

OBJECTIVE To determine the feasibility of radiographic measurement of liver area in small-breed dogs and to assess correlations between CT liver volume measurements (reference standard) and radiographic liver size measurements. ANIMALS 107 small-breed dogs (body weight, ≤ 10 kg) that had previously undergone orthogonal thoracic and abdominal radiography and abdominal CT. PROCEDURES In a retrospective study design, dogs were allocated to groups (normal liver [n = 36], microhepatia [34], and hepatomegaly [37]) on the basis of radiographic liver size and clinicopathologic findings. Radiographic liver area (RLA) was automatically calculated from archived radiographic images by free-hand outlining of the liver margins by use of DICOM viewer software, and other standard radiographic measurements were performed. Liver volume was measured on CT images. Intraoperator repeatability of RLA and CT measurements was assessed (duplicate measurements 2 weeks apart). To control for various breed conformations, radiographic values were normalized to body weight and T11 area. RESULTS Mean ± SD ratios of RLA to T11 area and RLA to body weight for dogs with normal livers were 32.7 ± 6.2 and 7.0 ± 1.4, respectively. Excellent intraobserver agreement was observed in RLA measurements within groups (intraclass correlation coefficients, 0.861 to 0.989), and RLA measurements had the highest correlation with CT liver volume measurements (r = 0.94) of all radiographic measurements. CONCLUSIONS AND CLINICAL RELEVANCE Findings indicated that RLA measurement in small-breed dogs with or without liver disease was useful and accurate for estimation of liver size, compared with CT measurement, and might be particularly useful for monitoring of changes in liver size.

Inclusion body hepatitis (IBH) has been reported in many countriesin the world. The IBH characterized presence of intra-nuclear inclusion bodies in hepatocytes in chickens. On December 2015, an onset of high acute mortality in a flock of 12, 18 and 23- day-old broiler chickens in Malacca and Johore was reported to the RegionalVeterinary Laboratory, Johor Bahru, Peninsular Malaysia. The birds showed lethargy, huddling, ruffled feathers, and inappetence. At necropsy, the livers were enlarged, pale yellow, friable andwith multiple petechial hemorrhages, the kidney were congested and enlarged, with hydropericardium and gizzard erosion. Large eosinophilic intranuclear inclusion bodies were seen in hepatocytes. PCR revealed liver were positive of FAdV at expected band of 1219 bp and the nucleotide sequence share 95-99% identity with the fowl adenovirus species E, serotype 8b. Based on the acute high mortality, age of the broilers, gross and microscopic lesions (especially intranuclear inclusion bodies) and molecular finding, the condition was diagnosed as adenovirus inclusion body hepatitis.

The accuracy of ultrasonography in detection of feline hepatic lipidosis was studied retrospectively. The following ultrasonographic criteria were associated positively with severe hepatic lipidosis: the liver hyperechoic, compared with falciform fat; the liver isoechoic or hyperechoic, compared with omental fat; poor visualization of intrahepatic vessel borders; and increased attenuation of sound by the liver. In a group of 36 cats with clinically apparent hepatobiliary disease and in which liver biopsy was done, liver hyperechoic, compared with falciform fat, was the best criterion for diagnosis of severe hepatic lipidosis with 91% sensitivity, 100% specificity, and 100% positive predictive value.

Alterations in serum lipid and lipoprotein concentrations in ponies with experimentally induced liver disease were investigated. Hepatocellular damage was induced, using a nonlethal dose of carbon tetrachloride. In a separate group of ponies, obstructive jaundice was induced by surgical ligation of the common bile duct. Over a 6-day period, blood samples were obtained from ponies after treatment with carbon tetrachloride and for 12 days in ponies subjected to surgery. Serum cholesterol and triglyceride concentrations were unaffected in both groups of ponies, except for significantly (P < 0.01) high triglyceride concentration in ponies of the ligated group during the second postsurgical week. This increase was most likely attributable to anorexia observed during that period. Hyperbilirubinemia was observed early in ponies of the ligated group; most of the bilirubin was of the conjugated type. Using electrophoretic and ultracentrifugal methods, serum lipoprotein alterations were detected only in ponies of the ligated group. Increases of very low-density and low-density hpoprotein cholesterol concentrations and decrease in high-density lipoprotein cholesterol concentration were found. Although no changes were seen in total serum cholesterol concentration, a redistribution of lipoprotein cholesterol was observed in ponies of the ligated group. Similar alterations in lipoprotein distribution have been found in dogs, rats, and human beings with obstructive jaundice and cholestasis. The association between serum lecithin:cholesterol acyl transferase activities and these lipoprotein alterations remains to be elucidated.

The size of the liver, as well as the situation and diameter of vessels in cattle were determined by use of ultrasonography. Ultrasonographic examinations of the liver were performed on 10 cows 10 times within 2 weeks, using a 3.5-MHz linear transducer on the right side in the 12th, 11th, and 10th intercostal spaces. Dorsal and ventral margin of the liver as well as localization and diameter of the caudal vena cava and the portal vein were determined in each intercostal space. Furthermore, the angle of the liver in the ventral area between the visceral surface and the diaphragmatic surface, the dorsal margin, and the circumference of the gall bladder were determined. The ultrasonographic values of liver size and localization in healthy cows can be used as reference values for the diagnosis of changes in liver size attributable to illness.

To differentiate the origin of high total lactate dehydrogenase (LD) activity in canine sera, a spectrophotometric method based on the preferential inhibition of cardiac LD isoenzymes by pyruvate was performed. Comparison with the electrophoretic separation of LD isoenzyme activities and determination of the hydroxybutyrate dehydrogenase-to-LD ratio indicated that the method proposed gave a better discrimination between cardiac and hepatic LD activities than did the other tests.

Protein kinase (PK) C activity in the liver of cattle with fatty liver syndrome was evaluated and compared with that in liver of healthy cattle. The PKC activities in cytosolic and particulate fractions were reduced in fatty livers, compared with those in livers from healthy cattle. The decrease of PKC activity was more distinct in cytosolic (P = 0.0016) than particulate (P = 0.069) fractions. Protein kinase activities other than PKC were not substantially changed. Seemingly, PKC was involved in the pathogenesis of fatty liver syndrome in cattle.