Ammonia Tolerance Test Research Articles

Ammonia and salinity tolerance of Penaeus monodon across eight breeding families.

Ammonia nitrogen and salinity tolerance of Penaeus monodon from eight selected breeding families were evaluated at the concentration of 67.65 mg L−1 ammonia-N and reducing salinity from 15 to 0 ‰. The final survival of family A (88.67 ± 9.81 %) was highest, and the final survival of family B was lowest (24.33 ± 14.01 %) after the ammonia tolerance test. Upon completing the sudden drop salinity test from 15 to 0 ‰, the highest survival was observed in family B (98.00 ± 1.73 %), and the lowest survival was found in family H (18.00 ± 1.73 %). Family A showed the strongest ability to tolerate ammonia stress, and family B showed the strongest tolerance to low salinity. This study suggests that the tolerance of salinity and ammonia nitrogen varied between breeding families. Results from the present study provide useful information towards selective breeding in shrimp in aquaculture for environmental tolerance.

Diagnostic value of the rectal ammonia tolerance test, fasting plasma ammonia and fasting plasma bile acids for canine portosystemic shunting

Portosystemic shunting (PSS) often results in hyperammonaemia and, consequently, hepatic encephalopathy. This retrospective study evaluated the sensitivity, specificity, positive and negative predictive values (PPV and NPV, respectively) and other test performance metrics for the ammonia tolerance test (ATT), serum fasting bile acids (FBA), serum fasting ammonia concentration (FA), and combinations of these tests for their association with PSS in dogs. Medical records of 271 dogs suspect for PSS (symptomatic group) and 53 dogs returning for evaluation after surgical closure of a congenital PSS (CPSS post-surgical control group) were analysed.In the symptomatic group, ATT at 40 min (T40), and the FBA had the highest sensitivity (100% and 98%, respectively) and NPV (100% and 96%, respectively) for PSS. The combination of increased FBA and FA had the highest specificity (97%), with a PPV of 97%, and a positive likelihood ratio of 29. In the CPSS post-surgical control group, the specificity and PPV of FA and the combination of increased FBA/FA were both 100%. In purebred populations, the NPV of all tests was 100%. Consequently, PSS would be ruled out in a symptomatic dog with normal FBA or ATT (T40) and would be highly probable when both FBA and FA are increased. Increased FA was conclusive for PSS in dogs evaluated for post-surgical closure of a CPSS. FBA was the most suitable test for screening purposes.

Recombinant hepatocyte growth factor treatment in a canine model of congenital liver hypoplasia

Although the liver has a large regenerative capacity, in many hepatopathies, these repair mechanisms fail. The therapeutic potential of hepatocyte growth factor (HGF) has been proven in numerous toxin-induced liver failure models in rodents, but never in spontaneously occurring liver diseases in larger animal models. The aim of this study was to induce liver growth in a hypoplastic liver by the administration of exogenous recombinant HGF. The natural hypoplastic liver model used is the canine congenital portosystemic shunt (CPSS) characterized by strongly reduced liver growth and function. Recombinant HGF (rHGF), 200 μg/kg, was given twice daily during 3 weeks by an intravenous injection in six dogs with CPSS. Liver volumes were determined by computed tomography before and at 1, 2, 3 and 7 weeks after the initiation of treatment. Portosystemic shunting was evaluated with an ammonia tolerance test and liver portal perfusion was quantified with scintigraphy. Simultaneously, blood parameters for liver function were assayed and liver biopsies were taken for histology, immunohistochemistry and gene-expression measurements. During 3 weeks of HGF treatment, hepatocyte proliferation increased and an increase in liver volume up to 44% was seen, persisting in two dogs up to 4 weeks after the termination of treatment. Ki-67 expression, gene expression of E2F1 and CDC6, phosphorylated-c-MET and phosphorylated-ERK1/2 protein levels confirmed increased hepatocyte proliferation and HGF signalling. The aberrant portal perfusion did not change during treatment. Transient in vivo liver growth is shown using CPPS as a naturally occurring large animal model, indicating the therapeutic potential of HGF in liver disease.

Hyperammonaemia in V1a vasopressin receptor knockout mice caused by the promoted proteolysis and reduced intrahepatic blood volume.

An analysis of arginine-vasopressin (AVP) V1a receptor-deficient (V1aR-/-) mice revealed that glucose homeostasis and lipid metabolism were altered in the mutant mice. Here, we used V1aR-/- mice to investigate whether the deficiency of the V1a receptor, which led to altered insulin sensitivity, affected protein metabolism. The serum 3-methylhistidine levels were increased in V1aR-/- mice under feeding conditions, indicating that proteolysis was enhanced in muscle tissue from V1aR-/- mice. Furthermore, serum amino acid profiling revealed that the amino acid levels, including glycogenic and branched-chain amino acids, were reduced in V1aR-/- mice. In addition, an alanine-loading test showed that gluconeogenesis was enhanced in V1aR-/- mice. Blood ammonia, which is a by-product of amino acid catabolism, was two times higher in V1aR-/- mice without hepatopathy under the feeding and fasting conditions than in wild-type mice. Amino acid profiling also revealed that the amino acid pattern was not typical of a urea-cycle enzymatic disorder. An ammonia tolerance test and an indocyanine green elimination test showed that V1aR-/- mice had lower ammonia clearance due to a decreased intrahepatic circulating blood volume. Metabolic acidosis, including lactic- and keto-acidosis, was not observed in V1aR-/- mice. These results provide evidence that proteolysis promotes the production of glucose in the muscles of V1aR-/- mice and that hyperammonaemia is caused by promoted protein catabolism and reduced intrahepatic blood volume. Thus, our study with V1aR-/- mice indicates that AVP plays a physiological role via the V1a receptor in regulating both protein catabolism and glucose homeostasis.

Hyperammonaemic encephalopathy secondary to selective cobalamin deficiency in a juvenile Border collie

An eight-month-old Border collie was presented with anorexia, cachexia, failure to thrive and stupor. Laboratory tests demonstrated a mild anaemia, neutropenia, proteinuria and hyperammonaemia. Serum bile acid concentrations were normal, but an ammonia tolerance test (ATT) was abnormal. The dog responded to symptomatic therapy for hepatoencephalopathy. When a low serum cobalamin (vitamin B12) concentration and methylmalonic aciduria were noted, the dog was given a supplement of parenteral cobalamin. Two weeks later, a repeat ATT was normal. Cobalamin supplementation was continued every two weeks, and all clinical signs, except for proteinuria, resolved despite withdrawing all therapy for hepatoencephalopathy. A presumptive diagnosis of hereditary selective cobalamin malabsorption was made, based on the young age, Border collie breed, low serum cobalamin concentration and methylmalonic aciduria. Although hereditary selective cobalamin malabsorption in Border collies, giant schnauzers, Australian shepherd dogs and beagles has previously been reported in North America, to the authors' knowledge this is the first report of the condition in the UK and the first to document an abnormal ATT in a cobalamin-deficient dog.

Postprandial Venous Ammonia Concentrations in the Diagnosis of Hepatobiliary Disease in Dogs

A postprandial ammonia tolerance test (PPATT) was performed on normal dogs and dogs with signs that suggested they may have liver disease. All dogs underwent transcolonic scintigraphy, liver biopsy, or both and were assigned to extrahepatic disease, primary hepatocellular, and congenital portosystemic vascular anomalies (PSVA) groups. Each dog was fed a chicken and rice diet providing 25% of its estimated daily metabolizable energy requirement (MER) as an ammonia challenge. This is practical in patients with liver disease because ammonium chloride administration often causes vomiting or ammonia toxicity. Venous ammonia concentrations were measured before feeding and every 2 hours after feeding for 8 hours. No difference in mean ammonia concentrations between dogs with extrahepatic disease and control dogs was found. Therefore, the specificity of the PPATT was 100%. Dogs with hepatocellular disease showed no change in mean ammonia concentration at any time point, before or after feeding, but sensitivity was greatest when venous ammonia was measured 6 hours after feeding (sensitivity before feeding, 28%, and after feeding, 36%). Among dogs with congenital PSVA, mean ammonia concentrations were higher than the reference range at all time points before and after feeding, and peak mean ammonia concentration occurred 6 hours after feeding. In this group, the sensitivity of the PPATT was 81% before feeding and 91% 6 hours after feeding. This study demonstrates that the measurement of venous ammonia concentration is a useful test to detect congenital PSVA, and the sensitivity of the test may be improved by sampling 6 hours after feeding. The PPATT has poor sensitivity in detecting primary hepatocellular disease.

Post-prandial serum bile acid concentrations and ammonia tolerance in Maltese dogs with and without hepatic vascular anomalies.

Post-prandial serum bile acid concentrations were measured in 200 Maltese dogs in an attempt to identify those with subclinical portosystemic shunts. Five of these were later shown to have hepatic pathology or abnormal liver function. In the other 195 Maltese, bile acid concentrations ranged from 1 to 362 mumol.L-1 (mean +/- SD, 70 +/- 50 mumol.L-1; median, 65.0 mumol.L-1). Of these, 79% were above the reference range (0 to 31 mumol.L-1) established from 23 mixed-breed control dogs. It was therefore not possible to determine the prevalence of subclinical portosystemic shunts on the basis of bile acid determinations. Further investigation of liver function was performed to investigate why bile acid concentrations were increased in these dogs. Rectal ammonia tolerance tests were normal in 102 of 106 Maltese tested and liver samples (11 dogs) and plasma biochemistry profiles (9 dogs) demonstrated no significant hepatic disease or dysfunction. Of 2 Maltese with hyperammonaemia after administration of ammonium chloride, one had a large congenital portosystemic shunt that was confirmed at surgery. In the other there were no macroscopic portosystemic communications, but a liver biopsy showed histological changes consistent with microscopic portovascular dysplasia. Total serum bile acid concentrations were consistently lower when assessed by high-performance liquid chromatography than by an enzymatic spectrophotometric method. This discrepancy was substantially larger in Maltese than in control dogs, suggesting the presence of an additional reacting substance in the serum of Maltese dogs.

犬の門脈大静脈短絡の1治験例

A 1-year-old, female, Shiba dog showed head tremors, staggering and depression, blindness, seizure and a coma. These signs progressed over a very short time. Serum biochemical data revealed increased ammonia, GPT and ALP, and abnormal urological findings of ammonium biurate were present. Portocaval shunt could be diagnosed tentatively and medical management with fluid therapy was carried out but no clinical improvement was observed. Portocaudalcaval shunt was diagnosed by operative portography and a 4F flexible catheter was inserted into the caudal vena cava through the shunt vessel. During operation, it was detected that the shunt vessel was branched just before the caudal vena cava. Portal vein pressure was measured during shunt vessel ligature and a total occlusion was performed because of a marked increase in the portal vein pressure was not observed. Palpation of the inserted catheter as it passed between the mesenteric and portal veins, and through the shunt identified the surgical location. Clinical improvement was generally noted within the first two days postperation and an ammonia tolerance test revealed excellent results.

Hepatotoxicity of phenobarbital in dogs: 18 cases (1985-1989)

Summary The medical records of 18 dogs that had hepatic disease and received phenobarbital as an anticonvulsant for 5 to 82 months were reviewed. Clinical signs included sedation and ataxia in all dogs, 5 dogs were also anorectic, 2 had coagulopathy, 3 were icteric, and 5 had ascites. Serum biochemical analysis revealed serum albumin concentration ≤ 2.2 g/dl in 12 dogs, serum alkaline phosphatase activity ≥ 169 U/L in 18 dogs, serum alanine transaminase activity ≥ 57 U/L in 15 dogs, and total bilirubin concentration ≥ 1 mg/dl (in the absence of lipemia) in 7 dogs. Serum phenobarbital concentration was ≥ 40 μg/ml in 12 of 17 dogs. Sulfobromophthalein excretion was prolonged in 8 of 10 dogs. Preprandial serum bile acid concentrations were high in 8 of 10 dogs, and 2-hour postprandial serum bile acid concentrations were high in 9 of 10 dogs. Two of 4 dogs tested had resting plasma ammonia concentrations > 200 mg/dl. An ammonia tolerance test was performed on 2 other dogs; both had ammonia concentration ≥ 200 mg/dl in the plasma 30 minutes after receiving 100 mg of ammonium chloride/kg of body weight, po. Nine dogs died, 1 was euthanatized, and necropsies were performed on these 10 dogs. Biopsies and necropsies of 6 dogs revealed chronic hepatic fibrosis with nodular regeneration (cirrhosis). One dog had hepatocellular carcinoma and mild cirrhosis. In 1 dog, after phenobarbital had been withheld, necropsy revealed complete recovery of the previously observed lesions.

The ammonia tolerance test in horses

Clinically normal horses (n = 8) with ages ranging from 5 to 8 years, were starved for 12 h and their plasma ammonia concentrations were measured. The mean fasting plasma ammonia concentration was 17.8 +/- 3.8 mumol l-1. After dosing ammonium chloride at a dose rate of 0.02 g kg-1, there was a significant increase in plasma ammonia concentration, with a maximum rise after 20 min (P less than 0.05). To investigate the influence of temperature on plasma ammonia concentrations of stored samples, 8 plasma samples were stored at -20 degrees C and 4 degrees C respectively. The plasma ammonia concentrations were measured after 6, 12 and 24 h in each of the stored samples. Plasma ammonia concentrations increased significantly after 12 and 24 h when stored at 4 degrees C (P less than 0.05). When plasma was stored at -20 degrees C there was no significant increase from baseline concentrations during 24h (P greater than 0.05).

The Effects of Ammonia Tolerance Tests on the Cerebrospinal Fluid Concentrations of Amino Acids and Indoleamines in Patients with Liver Cirrhosis

To study the effect of ammonia administration on amino acids and indoleamines in cerebrospinal fluid (CSF) and on amino acids, insulin, and glucagon in plasma in humans with liver cirrhosis, we performed seven ammonia tolerance tests on six patients with stable liver cirrhosis. The grade of encephalopathy was determined by psychometric tests. Only one of the patients had pronounced encephalopathy. The other patients had no or only slight encephalopathy. The plasma concentrations of valine, leucine, isoleucine, phenylalanine, tyrosine, and methionine decreased after the ammonia load, whereas no changes were found in the plasma concentrations of glucagon and insulin. In CSF the concentrations of glutamine, aromatic amino acids, and indoleamines increased only in the patient who had pronounced encephalopathy, whereas no changes were found in the other patients. The effect of an ammonia load on the concentrations of neutral amino acids in CSF in patients with pronounced encephalopathy remains to be demonstrated.

Biochemical Evaluation of the Hepatobiliary System in Dogs and Cats

The causes and clinical signs of hepatobiliary involvement in disease are many and varied and often are not referable directly to this organ system. Laboratory investigation frequently is necessary to rule hepatic disease in or out, to assess the functional impact on the liver, and to decide whether hepatic disease is the patient's primary problem or a complication of something else. The selection and interpretation of laboratory tests to resolve these problems is based on an understanding of relevant functional anatomy and pathophysiology. The mainstay of such assessment is hepatic enzymology, which can detect active disease in both hepatocytes and the biliary system. The hepatocellular pattern of disease is characterized by increases in leakage enzymes such as SDH, GLDH, and ALT and the cholestatic pattern by increases in induced enzymes (ALP and GGT). In general, enzymology does not allow the intensity or functional effect of hepatobiliary disease to be assessed, and quite severe hepatopathies may have only minimal enzyme abnormalities. For this reason, the primary biochemical data base for ruling hepatobiliary disease in or out always should involve some screening tests of hepatic function, such as albumin, protein, bilirubin, glucose, or urea determinations; as well as urinalysis to search for bilirubinuria and urobilinogenuria in hyperbilirubinemic patients and for ammonium biurate crystals when hyperammonemia or hepatic encephalopathy is suspected. Because the liver synthesizes most clotting factors, evaluation of blood coagulation is indicated when surgery is contemplated on patients with liver disease or when bleeding is present. Paired pre- and post-prandial determinations of serum bile acids are the preferred method for assessment of hepatobiliary function in dogs and cats. However, the BSP clearance test continues to be useful in the functional assessment of the liver as long as the dye remains available to veterinarians. Clearance of BSP is delayed in hepatocellular, cholestatic, and portosystemic disease as well as by severe extrahepatic circulatory disturbances, In general, this functional test is less sensitive than serum bile acids or the ammonia tolerance test in the recognition of hepatic encephalopathy caused by portosystemic anomalies. The objectives of biochemical screening of the liver are to establish the type (hepatocellular, biliary, or mixed), duration (acute, chronic), and stage (aggressive, convalescent) of hepatobiliary disease and to assess functional status.(ABSTRACT TRUNCATED AT 400 WORDS)

Ammonia Tolerance Test Used to Differentiate between Ascites of Cirrhotic and Malignant Genesis

Eighteen patients with ascites, 9 with cirrhosis of the liver and 9 with malignant disease, were subjected to the ammonia tolerance test by instillation of ammonia transrectally . Arterial blood samples were taken before and 15 and 30 min after the instillation to determine the plasma ammonia concentrations. The results show a significant difference in the plasma ammonia concentration between the two groups of patients after instillation of ammonia. Since the method is non-invasive, it is recommended as a screening test in the differentiation between ascites of cirrhotic and malignant genesis.

Rectal ammonia tolerance test in the evaluation of portal circulation in dogs with liver disease

An ammonia tolerance test (ATT) is described in control dogs and in patients affected by liver disease with or without portosystemic collateral circulation. The administration of a 5 per cent ammonium chloride solution rectally proved to be preferable to oral administration. A statistically significant difference was shown between the results of the ATT in patients with and those without portal shunts, but not between control dogs and patients without portal collateral circulation. A simplified ATT is proposed in which venous ammonia determinations are made before and 20 and 40 minutes after rectal administration of 5 per cent ammonium chloride solution at a dose of 2 ml/kg bodyweight.

Ammonia-induced changes in pancreatic hormones and plasma amino acids in patients with liver cirrhosis.

The contribution of hyperammonemia to plasma amino acid imbalance in patients with liver disease was assessed in 10 subjects with chronic hepatitis and in 17 advanced cirrhotics. Insulin, glucagon, and plasma amino acids were determined both in the basal state and 45 min after oral ammonium chloride, at doses used in the ammonia-tolerance test. In cirrhotics, ammonia increased to 3 times basal values, in association with a rise in insulin and, more marked, in glucagon. Aromatic amino acids and free tryptophan further increased, while a significant fall in branched-chain amino acids and glutamate was observed. The increase in ammonia levels strongly correlated with the increase in glucagon (r = 0.707). Two patients, with large esophageal varices, showed signs of disturbed consciousness, in association with a marked rise in ammonia and in the ration of free tryptophan to the sum of neutral amino acids. In patients with chronic hepatitis, whose ammonia levels rose slightly, minor variations in pancreatic glucoregulatory hormones and plasma amino acids were observed, as also happened in 10 healthy subjects following ammonium chloride ingestion. Our data fit with the hypothesis that the plasma amino acid imbalance of cirrhotics may be partly due to ammonia-induced changes in pancreatic hormones.

Temporary beneficial effect of arterialization of the liver in cirrhotic dogs with a portacaval shunt. A preliminary report.

The effect of arterialization of the portal vein was investigated in cirrhotic dogs with a portacaval shunt. In dogs receiving a portacaval shunt only (PCS), the pressure in the intrahepatic portal vein fell to about 10% of the preshunt value, while the total hepatic blood flow was reduced by 63.9%. By contrast, in dogs with arterialization in addition to a portacaval shunt (PCS + A), the pressure in the portal vein was almost restored to preshunt levels, and the decrease in total hepatic blood flow was only 35.7%; this difference in the reduction of hepatic perfusion is significant (p less than 0.01). 2 weeks after the operation, PCS + A dogs had lower plasma levels of bilirubin and alkaline phosphatase, and a higher antipyrine clearance than PCS dogs (p less than 0.05). This improvement, however, was of short duration. The results of the ammonia tolerance test were not affected by the arterialization procedure.

Plasma amino acids as markers of liver dysfunction in cirrhotics.

To determine the role of liver dysfunction in the plasma amino acid profile of cirrhotic patients, we correlated basal plasma amino acids and several biochemical and functional hepatic variables in 29 cirrhotics with normal mental state or mild encephalopathy. Increased levels of aromatic amino acids and free tryptophan correlated positively with the extent of portosystemic shunt, as assessed by the ammonia tolerance test (r = 0.758 and r = 0.589, respectively). There was a negative correlation between these amino acids and liver function, as evaluated by the galactose elimination capacity test (r = -0.657 and r = -0.551), thus suggesting that phenylalanine, tyrosine, and free tryptophan may be considered indexes of liver dysfunction in non-comatose cirrhotics.

Oral ammonia tolerance test in patients with portal hypertension.

Eighty patients with portal hypertension due to various hepatic diseases were subjected to the oral ammonia tolerance test (OATT). Blood samples were collected before and at 30-min intervals after the administration of ammonium chloride (50 mg/kg). The ammonia levels, and the OATT curve patterns and sigma NH3-N values were determined and it was investigated whether there are correlations between these values and various other parameters of hepatic function. The results of OATT correlated with the plasma disappearance rate of indocyanine green and the molar ratio of branched chain amino acids to aromatic amino acids. Our findings suggest that the OATT may reflect the degree of hepatic parenchymal disorders rather than the hepatic circulatory abnormalities and that they may represent a valuable aid in the differential diagnosis of hepatic diseases and in determining the operative indication.

Morphology and function of isolated hepatocytes transplanted into rat spleen.

Hepatocytes isolated by the collagenase digestive method were transplanted into the spleens of syngeneic rats. Morphology and function of the hepatocytes in the spleen were investigated for 12 to 17 months after transplantation. The transplanted hepatocytes proliferated and reconfigured in the spleen without direct perfusion of portal venous blood and with the presence of an intact host liver. Fourteen to 17 months after transplantation, the hepatocytes which had formed a demarcated nodule occupied approximately 40% of the area of the splenic parenchyma without undifferentiation on microscopic examination. However, the weight of the hepatized spleen did not increase beyond the weight of a normal spleen and the weight of the host liver that had normal morphology also did not differ from a normal liver. Light and electron microscopic studies demonstrated differentiated cord structure and normal architecture for each heptocyte. Furthermore, the hepatized spleen synthesized albumin and glycogen as demonstrated by immunofluorescence and histochemical studies. Ammonia tolerance and indocyanine green clearance tests revealed functioning hepatocytes in the spleen proper. These results indicate that our experimental model lends itself well to investigations in cell growth mechanism and that hepatocellular transplantation has potential clinical application to compensate for impaired hepatic function.

Decontamination of corn containing aflatoxin by treatment with ammonia

AbstractCorn containing aflatoxin can be effectively decontaminated by treatment with gaseous ammonia at atmospheric pressure. Preliminary studies were made of the effect of ammonia level, corn moisture, temperature, and time on the aflatoxin level. Ammonia tolerance tests were carried out on laying hens as were acceptance tests by swine. Toxicity feeding trials with ducklings, broiler chicks, and trout confirmed that the process inactivates the aflatoxin. The process was then applied under farm scale conditions to produce materials for feeding trials with swine, poultry, and cattle under FDA protocols. The process can reduce aflatoxin levels from 1000 parts per billion (ppb) to within the FDA action level of 20 ppb.