Blood Ammonia Concentration Research Articles

Combined Analysis of Blood Ammonia and Lactate Levels as a Practical Tool to Assess the Metabolic Response to Training Sessions in Male and Female Sprinters.

Kantanista, A, Kusy, K, Pospieszna, B, Korman, P, Wieliński, D, and Zieliński, J. Combined analysis of blood ammonia and lactate levels as a practical tool to assess the metabolic response to training sessions in male and female sprinters. J Strength Cond Res 35(9): 2591-2598, 2021-Previous research has mainly focused on blood ammonia and lactate concentration changes in response to exercise in laboratory settings. The aim of this study was to present a combined analysis of blood ammonia and lactate levels obtained during various training sessions performed under real training conditions. Differences between the sexes were also analyzed. The study subjects included 9 male and 8 female sprinters competing at the international level. The two-way analyses of variance, with repeated measures (time × sex), for lactate and blood ammonia concentrations during strength, speed (only lactate), speed with baton exchange, and speed endurance training sessions were significant. Blood ammonia and lactate levels obtained during repeated sprints were higher in male than female athletes. Peak lactate concentrations obtained from different training sessions were different in the female (F(3, 18) = 49.82, p ≤ 0.001, η2 = 0.893) and male (F(3, 21) = 312.26, p ≤ 0.001, η2 = 0.978) athletes; post hoc analyses of the men and women showed differences in maximum lactate concentration between training sessions, except in the speed and strength sessions. Peak ammonia concentrations obtained in the different training sessions were also different in the female (F(3, 18) = 121.06, p ≤ 0.001, η2 = 0.953) and male (F(3, 21) = 196.04, p ≤ 0.001, η2 = 0.965) athletes; in both the men and women, significant differences in maximum blood ammonia concentrations were found between the training sessions, except for the speed and speed with baton exchange training sessions. The results of this study indicate that the combined analysis of lactate and blood ammonia concentration provides the coach with valuable additional information about the level of adenosine triphosphate breakdown, the energy system contribution involved in muscle energy coverage during very short, repeated maximal sprints, and, most importantly, allows the coach to check whether preworkout goals were actually met.

Pharmacotherapies that specifically target ammonia for the prevention and treatment of hepatic encephalopathy in adults with cirrhosis.

Pharmacotherapies that specifically target ammonia for the prevention and treatment of hepatic encephalopathy in adults with cirrhosis.

Evaluation of VACUETTE® cat serum fast separator blood collection tube for routine chemistry assays

Background: Hyperammonemia is neurotoxic and as such can be a medical emergency. Preanalytical factors greatly influence the blood ammonia concentration results. Aims and methods: Ammonia concentrations measured in the real life setting of a large hospital after pneumatic transport of blood samples and various time periods before centrifugation were compared to those based on the indications of the reagent manufacturer. In the same routine context, the effects of waiting times of centrifuged samples or after plasma storage at −20 °C and −80 °C were determined. Results: Despite the pneumatic transport, the lead times for sample arrival to the lab were even longer than those recommended for their complete handling until ammonia assay. Ammonia concentration results were not affected by the pneumatic transport of blood samples and by waiting times up to a maximum of 1.75 h before their centrifugation and 1 h after centrifugation. Ammonia stability was superior when plasma was stored at −80 °C. Conclusion: Pneumatic transport and sample handling in the routine practice of our lab do not affect ammonia concentration results provided that waiting times are limited to 1.75 h before and 1 h after centrifugation and samples are kept cold. Otherwise, it is better to freeze plasma at −80 °C.

Plasma citrulline, arginine, nitric oxide, and blood ammonia levels in neonatal calves with acute diarrhea.

BackgroundPlasma citrulline (CIT) concentration is considered to be a reliable marker of functional enterocyte mass, primarily in humans. However, information about CIT levels along with related metabolites, arginine (ARG), nitric oxide (NO), and ammonia in neonatal calves are lacking.ObjectivesTo compare plasma CIT, ARG, NO, and whole blood ammonia concentrations in neonatal calves with acute diarrhea with those in healthy calves and to assess their possible relationships with diarrhea‐related criteria.AnimalsSeventy neonatal calves (60 with acute diarrhea and 10 healthy).MethodsObservational case‐control study. Diarrheic calves were classified into subgroups on the basis of etiology, severity of diarrhea, degree of dehydration, and systemic inflammatory response syndrome (SIRS) status. Plasma CIT and ARG concentrations were measured by liquid chromatography/tandem mass spectrometry.ResultsPlasma CIT (median [range]: 67.5 [61.9‐75.4] vs 30.1 [15.0‐56.1] μmol/L) and ARG (170.7 [148.5‐219.5] vs 106.1 [54.4‐190.7] μmol/L) were lower and plasma NO (4.42 [3.29‐5.58] vs 6.78 [5.29‐8.92] μM) and blood ammonia concentrations (28.7 [26.1‐36.9] vs 59.8 [34.6‐99.5] μmol/L) were higher in the neonatal calves with diarrhea (P < .001). Plasma CIT (β = −0.29, P = .02), ARG (β = −0.33, P = .01), NO (β = 0.55, P < .001), and blood ammonia (β = 0.63, P <.001) were affected by SIRS status. Except for ammonia (0.52), the effects sizes for severity of diarrhea and degree of dehydration were small (ηp2 ≤ 0.45) for CIT, ARG, and NO.Conclusions and Clinical ImportanceThe changes in these variables might have diagnostic, prognostic, and therapeutic value in diarrheic neonatal calves.

Demethylation of the hypoxia induction factor 1 binding site of GPX3 at excess blood ammonia in propionic acidemia

ObjectivesElevated levels of metabolites such as ammonia and propionylcarnitine in propionic acidemia (PA) lead to an increased reactive oxygen species (ROS) production which could activate and stabilize the epigenetic regulated hypoxia-inducible factor-1α (HIF-1α). In order to evaluate the DNA methylation status of the HIF-1α binding site in PA, we investigated the antioxidant gluthatione peroxidase 3 gene (GPX3) promoter region. Design and methodsUsing leukocyte DNA extracted from bloodspots collected 2–4 days after birth from diet free newborns, the cytosine phosphodiester bond guanine (CpG) dinucleotides of a HIF-1α binding site (CGTTTTTTACG) in the promoter region of GPX3 was retrospectively analysed. Patients included 7 PA.and 7 healthy controls (KO) respectively. ResultsA demethylated TGTTTTTTATG allele was detected in 3 PA patients with blood ammonia (NH3) concentrations of 500, 595, and 987 umol/L respectively; a demethylated/partial methylated TGTTTTTTAC/TG allele in 4 PA patients (2 PA with blood NH3 = 213, 271 umol/L respectively); a partial methylated C/TGTTTTTTAC/TG allele in 5 healthy controls respectively; a partial methylated/methylated C/TGTTTTTTACG allele in 2 healthy controls. ConclusionOur results suggest that at excess NH3, the DNA methylation status of the HIF-1α binding site of GPX3 in newborns with PA is demethylated (TGTTTTTTATG allele). However, the demethylated allele has to be confirmed as a statistically significant change in more patients.

Dietary leucine supplementation enhances the health of early weaned Hu lambs

This study investigated the effects of leucine supplementation on the performance of pre- and post-weaning of early weaned Hu lambs. Thirty lambs of five-day-old, with an average body weight of 3.60 ± 0.73 kg, were assigned randomly to the control or leucine group, with each group having 5 replicate pens. Lambs in the leucine group received 7.1 g/kg total feed dry matter leucine in milk replacer from 10 days of age onward. Blood samples were collected from one lamb of each replicate randomly to determine plasma metabolites, oxidative stress indicators and immunize variables when lambs were early weaned at 30 days of age. After weaning, one lamb of each replicate was kept in their same pen and fattened to 120 days old. These lambs (5 lambs per treatment) were slaughtered to determine the carcass traits and drip loss of muscle. Growth performance before weaning did not differ (P > 0.05) between the control and leucine group. Leucine supplementation increased (P < 0.05) plasma concentrations of asparagine, isoleucine and leucine, and total antioxidant capacity and glutathione peroxidase activity. Supplementation of leucine decreased (P < 0.05) concentrations of blood urea nitrogen, blood ammonia, and d-lactate. Compared to the control group, the leucine group achieved a higher dressing percentage (P < 0.05). Furthermore, leucine supplementation decreased (P < 0.05) the drip loss of mutton at both 24h and 48h. Collectively, these results indicate that leucine supplementation can enhance the antioxidant and immune status and help maintain the health of early weaned Hu lambs.

L-Carnitine for the Treatment of Overt Hepatic Encephalopathy in Patients with Advanced Liver Cirrhosis.

Hepatic encephalopathy is a major complication in patients with advanced cirrhosis and is associated with poor prognosis. To evaluate the effectiveness of L-carnitine supplementation in patients with overt hepatic encephalopathy (OHE), outcomes were retrospectively analyzed in patients with OHE who were treated with intravenous branched-chain amino acids (BCAA), with or without intravenous L-carnitine. Twenty-six patients were treated with intravenous BCAA in addition to conventional agents such as lactulose and non-absorbable antibiotics (Group A), and 19 patients were treated with these agents plus intravenous L-carnitine (Group L). Changes in blood ammonia concentrations, hepatic coma grade and the Glasgow Coma Scale (GCS) were compared in the two groups. Recurrence-free survival (RFS) was evaluated in the two groups and in patients who were and were not administered oral L-carnitine supplementation. At baseline, GCS scores were significantly lower and deterioration in liver function greater in Group L. After 3 d of intravenous L-carnitine, however, GCS showed a significantly greater improvement in Group L than in Group A. Blood ammonia levels improved stably over time in Group L. Overall survival and RFS were similar in Group L and Group A, but median RFS was significantly longer in patients who did than did not receive oral L-carnitine supplementation (735 versus 497 d, p=0.03). Although these findings are preliminary, L-carnitine supplementation may be a therapeutic option for patients with OHE and disturbed consciousness.

Jump height loss as an indicator of fatigue during sprint training

ABSTRACTThis study analysed the acute mechanical and metabolic responses to a sprint training session focused on maintaining maximal speed until a given speed loss was reached. Nine male high-level sprinters performed 60 m running sprints up to a 3% in speed loss with 6 min rests between sets. Mechanical responses (countermovement jump (CMJ) height and speed loss) and metabolic responses (blood lactate and ammonia concentrations) were measured pre-exercise and after each set was performed. Jump height loss showed almost perfect relationships with both lactate (r = 0.91) and ammonia (r = 0.91) concentrations. In addition, nearly perfect relationships were observed for each athlete between CMJ height loss and lactate (r = 0.93–0.99) and ammonia (r = 0.94–0.99). Very large correlations were found between speed loss and lactate (r = 0.83), and ammonia (r = 0.86) concentrations. Furthermore, close relationships were observed for each athlete between speed loss and lactate (r = 0.86–0.99), and ammonia (r = 0.88–0.98). These results suggest that the CMJ test may allow more accurate setting of training loads in sprint training sessions, by using an individualised sprint dose based on mechanical and physiological responses rather than a standard fixed number of sprints for all athletes.

Effect of tumor necrosis factor-\u03b1 on the expression of the ammonia transporter Rhcg in the brain in mice with acute liver failure

BackgroundAmmonia and tumor necrosis factor-alpha (TNF-α) play important roles in the mechanisms of hepatic encephalopathy (HE). Rhesus glycoprotein C (Rhcg) is important for ammonia transport especially in the kidney. The aim of the present study was to investigate the role of Rhcg in the brain in acute liver failure (ALF) and the effect of TNF-α on Rhcg expression.MethodsALF mouse models were generated by treatment with d-galactosamine (D-GalN) and lipopolysaccharide (LPS), or D-GalN and TNF-α. ALF induction was blocked by pretreatment with anti-TNF-α IgG. The levels of serum TNF-α were determined by ELISA. Blood ammonia and brain ammonia concentrations were detected using an ammonia assay kit. The expression and distribution of Rhcg in the brain tissues of ALF mice were examined by western blotting, real-time PCR, immunohistochemical, and immunofluorescence analyses.ResultsSerum TNF-α levels were increased in the LPS/D-GalN group. Blood and brain ammonia were increased in the LPS/D-GalN- and TNF-α/D-GalN-induced ALF groups. Rhcg mRNA and protein levels were elevated in both ALF groups, consistent with the increase in blood and brain ammonia. Rhcg was mainly expressed in vascular endothelial cells and astrocytes. Pretreatment with anti-TNF-α IgG antibody downregulated Rhcg in brain tissues in the LPS/D-GalN group, prevented the occurrence of ALF, and reduced blood and brain ammonia levels in the LPS/D-GalN group.ConclusionTNF-α promoted the transport of ammonia from the blood to brain tissues and exacerbated the toxic effects of ammonia by upregulating Rhcg.

Cross-over study in hyperammonemia patients for efficacy, safety, and acceptability of a new lactulose preparation (SK-1202) compared to approved drug.

A novel jelly lactulose preparation (SK-1202) has been developed to improve compliance and reduce the elevation of blood glucose levels in diabetic patients. To compare the equivalence in the efficacy and safety of SK-1202 and an approved commercially available syrup preparation, we undertook a randomized multicenter cross-over study in hyperammonemia patients with liver cirrhosis who were taking lactulose. Forty-four patients were enrolled and took each preparation for 2weeks. Efficacy was evaluated using the Number Connection Test, blood ammonia concentration, coma grade, and the flapping tremor grade. Safety was evaluated by the number of adverse events observed, vital signs, and laboratory tests. We also examined the acceptability of each preparation using questionnaires evaluating sweetness, aftertaste, ease of use, and preference of the preparations. There were no differences in efficacy or safety between SK-1202 and the approved syrup preparation. With regard to the acceptability evaluation, given over 80% of the participants chose the SK-1202 preparation, it appears to be preferred by patients. It is expected that SK-1202 could represent a useful agent for patients with hepatic encephalopathy.

Keto analogues and amino acid supplementation and its effects on ammonaemia during extenuating endurance exercise in ketogenic diet-fed rats.

Keto analogues and amino acids (KAAA) supplementation can reduce blood ammonia concentrations in athletes undergoing high-intensity exercise under both ketogenic and thermoneutral conditions. This study evaluated the acute effects of KAAA supplementation on ammonia metabolism during extenuating endurance exercise in rats fed a ketogenic diet. In all, eighty male Fischer rats at 90 d of age were divided into eight groups, and some were trained using a swimming endurance protocol. A ketogenic diet supplemented with keto analogues was administered for 10 d. Administration of the ketogenic diet ended 3 d before the exhaustion test (extenuating endurance exercise). A ketogenic diet plus KAAA supplementation and extenuating endurance exercise (trained ketogenic diet supplemented with KAAA (TKKa)) increased blood ammonia concentrations by approximately 50 % compared with the control diet (trained control diet supplemented with KAAA (TCKa)) and similar training (effect size=1·33; statistical power=0·50). The KAAA supplementation reduced blood urea concentrations by 4 and 18 % in the control and ketogenic diet groups, respectively, compared with the groups fed the same diets without supplementation. The trained groups had 60 % lower blood urate concentrations after TCKa treatment than after TKKa treatment. Our results suggest that KAAA supplementation can reduce blood ammonia concentrations after extenuating endurance exercise in rats fed a balanced diet but not in rats fed a ketogenic diet.

L-ornithine L-aspartate for prevention and treatment of hepatic encephalopathy in people with cirrhosis.

L-ornithine L-aspartate for prevention and treatment of hepatic encephalopathy in people with cirrhosis.

Changes in Blood pH and Ammonia Following Repeat Sprint Performance

The relationship between relative intensity and changes in blood pH and ammonia are not well characterized. PURPOSE: The primary aim of the study was to determine how changes in relative exercise intensity following repeat sprint performance affect changes in blood pH and blood ammonia concentrations. METHODS: Healthy college- age males (n = 12) completed completed one 30 second Wingate cycle sprint test as a familiarization trial. A minimum of 48 hours after the familiarization trial, participants returned to the lab. Resting venous and capillary blood samples were obtained to determine blood ammonia, pH, and lactate levels. Participants then completed 3 Wingate sprint tests, separated by 5 minutes each. Finger capillary blood was immediately obtained after each test to determine lactate and pH values. After the final test, an additional venous blood sample was obtained to determine blood ammonia values. RESULTS: Data are shown as 1st vs. 2nd vs. 3rd tests, respectively. There was a significant effect for time for peak power (750.08 ± 39.55 vs. 675.42 ± 30.01 vs. 615.60 ± 37.72 Watts); F = 4.66, p = 0.05, mean power (632.67 ± 30.71 vs. 561.25 ± 22.16 vs. 524.40 ± 26.46 Watts); F = 5.04, p = 0.04, pH (7.72 ± 0.01 vs. 7.63 ± 0.02 vs. 7.62 ± 0.02); F = 70.18, p < 0.01, and lactate (12.36 ± 1.14 vs. 14.10 ± 1.13 vs. 16.95 ± 1.22 mg/dL); F= 42.02, p < 0.01. Blood ammonia values did increase from pre- to post-exercise (0.33 ± 0.09 vs. 1.07 ± 0.22 mg/dl); t = 3.62, p < 0.01, but there was no correlation between post-exercise ammonia values and change in peak or mean power. There was a weak, but significant correlation between change in peak power and change in pH (R2 = 0.34, p = 0.05) and change in mean power and change in pH (R2 = 0.44, p = 0.02). CONCLUSIONS: Greater reductions in peak power and mean power correlated with change in blood pH, but not post-exercise ammonia values.

Efficacy and safety of rifaximin in Japanese patients with hepatic encephalopathy: A phase II/III, multicenter, randomized, evaluator-blinded, active-controlled trial and a phase III, multicenter, open trial.

The efficacy and safety of rifaximin in the treatment of hepatic encephalopathy (HE) are widely known, but they have not been confirmed in Japanese patients with HE. Thus, two prospective, randomized studies (a phase II/III study and a phase III study) were carried out. Subjects with grade I or II HE and hyperammonemia were enrolled. The phase II/III study, which was a randomized, evaluator-blinded, active-comparator, parallel-group study, was undertaken at 37 institutions in Japan. Treatment periods were 14 days. Eligible patients were randomized to the rifaximin group (1200 mg/day) or the lactitol group (18-36 g/day). The phase III study was carried out in the same patients previously enrolled in the phase II/III study, and they were all treated with rifaximin (1200 mg/day) for 10 weeks. In the phase II/III study, 172 patients were enrolled. Blood ammonia (B-NH3 ) concentration was significantly improved in the rifaximin group, but the difference between the two groups was not significant. The portal systemic encephalopathy index (PSE index), including HE grade, was significantly improved in both groups. In the phase III study, 87.3% of enrolled patients completed the treatment. The improved B-NH3 concentration and PSE index were well maintained from the phase II/III study during the treatment period of the phase III study. Adverse drug reactions (ADRs) were seen in 13.4% of patients who received rifaximin, but there were no severe ADRs leading to death. The efficacy of rifaximin is sufficient and treatment is well tolerated in Japanese patients with HE and hyperammonemia.

Diagnostic value of albumin-bilirubin grade combined with serum ammonia in cirrhosis with hepatic encephalopathy

Objective: To explore the value of albumin-bilirubin (ALBI) grade combined with serum ammonia in the diagnosis of cirrhosis with hepatic encephalopathy (HE). Methods: The serum level of total bilirubin(TBIL), albumin( ALB )and blood ammonia were detected in 139 patients including 73 cirrhosis patients without HE and 66 cirrhosis patients with HE from January 2015 to January 2017 in Beijing You'an Hospital, and the relationship between ALBI and blood ammonia value and Child grade and hepatic encephalopathy was analyzed. Results: The level of ALBI and blood ammonia were more and more higher with the increase of Child grade, the level of ALBI in Child A, B and C were -2.3±0.6, -1.7±0.5, -0.9±0.4, and there was a statistically significant(F=125.100, P<0.001). The blood ammonia concentration in Child A, B and C were(42.6±16.0), (56.1±31.2), (69.8±34.7) μmol/L, and there was a statistically significant(F=7.400, P<0.001). The level of ALBI was higher with the increase of model for end-stage liver disease (MELD) grade, and there was a positive correlation(r=0.547, P<0.001). The ALBI value in the HE group was higher than the cirrhosis patients without HE((-1.1±0.5)vs(-1.6±0.7)), and the difference was statistically significant (t=5.244, P<0.001). Level of blood ammonia in the HE group was(83.6±39.5)μmol/L, which was higher than the level of cirrhosis patients without HE(42.9±17.0)μmol/L, and the difference was statistically significant (t=8.130, P<0.001) . When ALBI and blood ammonia were combined, the ROC curve area was 0.911, the sensitivity was 93.9%, the specificity was 93.2%. Conclusion: There is a significant diagnosis value and high clinical application when ALBI is combined with blood ammonia to diagnose HE .

What is the real utility of breath ammonia concentration measurements in medicine and physiology?**We dedicate this article, intended for inclusion in the 10th Anniversary issue of the Journal of Breath Research, to the late Professor Dr Anton Amann, a close colleague and friend. This is particularly appropriate, because it was Anton’s initiative that brought the journal into being and his

Much effort continues to be devoted to the development of devices to analyse breath ammonia with the anticipation that breath ammonia analyses will be useful in clinical practice. In this perspective we refer to the analytical techniques that have been used to measure breath ammonia, focusing on selected ion flow tube mass spectrometry, SIFT-MS, of which we have special knowledge and understanding. From the collected data obtained using the different techniques, we exam the origins of mouth- and nose-exhaled ammonia and conclude that mouth-exhaled ammonia is always elevated above a concentration that would be equilibrated with blood ammonia and is largely produced by the action of enzymes on salivary urea. Support to this conclusion is given by the reasonable correlation between blood urea concentration and mouth-exhaled ammonia concentration. Further, it is discussed that nose-exhaled ammonia largely originates at the alveolar interface and so its concentration more closely relates to the expected alveolar blood ammonia concentration. Ingestion of proteins results in increased blood/saliva urea and ultimately mouth-exhaled ammonia as does the generation of urease by H. pylori infection. It is also concluded that when mouth-exhaled ammonia is elevated then it may be due to either abnormally high blood urea, a high pH of the saliva/mouth/airways mucosa, poor oral hygiene or a combinations of these.

How does the snakehead Channa argus survive in air? The combined roles of the suprabranchial chamber and physiological regulations during aerial respiration.

ABSTRACTThis study aimed to test the hypothesis that the aerial survival of the northern snakehead is involved not only with suprabranchial chamber respiration but also with physiological regulations. The aerial survival time and oxygen consumption rate (VO2) were determined in snakeheads with either normal or injured suprabranchial organs. Some hematological and biochemical parameters were assessed during aerial exposure. The results showed that resting VO2 decreased when switching from water to air in both the control and the suprabranchial organ-injured fish, with decreases of 22.4% and 23.5%, respectively. Resting VO2 in air was not different between the control and the suprabranchial organ-injured fish. The red blood cell (RBC) count and hemoglobin concentration showed no marked changes, while RBC size increased when exposed to air. The liver lactate concentration remained unchanged, and the white muscle lactate concentration decreased when switching from water to air. The blood ammonia concentration tended to increase during aerial respiration. These results suggest that the aerial survival of the snakehead is positively associated with a combination of factors, including respiration of suprabranchial organs and other accessory organs, depressed metabolic demands and increased oxygen transport, and negatively associated with the accumulation of blood ammonia but not anaerobic metabolism.

Modern view on hepatic encephalopathy: basic terms and concepts of pathogenesis

Background. The problem of acute and chronic forms of hepatic encephalopathy (HE) is not clearly identified among modern problems of hepatology and neuroscience in Ukraine. Despite the significant contribution to the development of lethal complications in patients with liver pathology and long history of the study of this issue, there is still no unified opinion on the links of HE pathogenesis.The aim of this review is to conduct a comprehensive analysis of current data on the spreading and mechanisms of development of HE.HE is a complex of potentially reversible neurocognitive disorders in patients with chronic or acute hepatic failure (ALF). HE is more often a complication of liver cirrhosis and is the second most frequent cause of hospitalization of such patients after ascites. When decompensating liver failure in acute or chronic hepatic pathology in patients severe forms of HE develop, accompanied by a progressive increase in intracranial pressure and the development of coma, which often ends lethal due to poor corrigibility of intracranial hypertension while maintaining hepatogenic neurointoxication. HE is considered as the end result of the accumulation of a number of neurotoxic substances in the brain, among which are ammonia, mercaptans, short chain fatty acids, false neurotransmitters, gamma-aminobutyric acid, manganese. The most popular among the reasons for the development of HE is the neurotoxic theory of ammonia. Ammonia is subjected to detoxification in the liver, turning into urea, a smaller fraction with the participation of glutamine synthetase is used in the synthesis of glutamine in muscles, liver and astrocytes of brain. In case of hepatic dysfunction and/or portosystemic shunting, the concentration of ammonia in blood increases up to 10 times and the main load for its detoxification is shifted to myocytes and astroglia. In ALF glutamine overload of astrocytes occurs with a change in intracellular osmolarity and subsequent edema of astroglia, which is accompanied by the development of cytotoxic edema of the brain. In this case, in astrocytes damaging of mitochondrial respiratory chain occurs and mitochondrial insufficiency develops, as well as processes of nitrosative-oxidative stress and oxidation of astrocytic and neuronal RNA, disruption of gene expression, synthesis of neuro- and gliotransmitters and synaptic plasticity. The increased influx of aromatic amino acids into brain leads to the synthesis of false neurotransmitters, which worsens serotoninergic, GABA-ergic, dopaminergic and glutamatergic neurotransmission. Damage to the components of the blood-brain barrier leads to aggravation of the water imbalance, penetration of hematogenous cytokines, endotoxins and other products of systemic inflammatory reaction into the cerebral parenchyma and development of neuroinflammation, which makes an important contribution to the further progression of cerebral edema.Conclusions: despite a comprehensive study of the problem, many open questions remain in the pathogenesis of HE. Special attention should be paid to more detailed study of the mechanisms of formation and elimination of edematous changes in brain tissue on the background of hepatogenic intoxication and the development of a systemic inflammatory reaction, the role of astroglia and its water channels in these processes, as well as the mechanisms of damage to the blood-brain barrier.

Ammonia concentrations in arterial blood, venous blood, and cerebrospinal fluid of dogs with and without congenital extrahepatic portosystemic shunts

OBJECTIVE To compare ammonia concentrations in arterial blood, venous blood, and CSF samples of dogs with and without extrahepatic portosystemic shunts (EHPSS). ANIMALS 19 dogs with congenital EHPSS and 6 healthy control dogs. PROCEDURES All dogs underwent a physical examination and then were anesthetized for transsplenic portal scintigraphy to confirm the presence or absence of EHPSS. While dogs were anesthetized, arterial and venous blood samples and a CSF sample were simultaneously collected for determination of ammonia concentration, which was measured by use of a portable blood ammonia analyzer (device A) and a nonportable biochemical analyzer (device B). Results were compared between dogs with EHPSS and control dogs. RESULTS Arterial, venous, and CSF ammonia concentrations for dogs with EHPSS were significantly greater than those for control dogs. For dogs with EHPSS, ammonia concentrations in both arterial and venous blood samples were markedly increased from the reference range. There was a strong positive correlation between arterial and venous ammonia concentrations and between blood (arterial or venous) and CSF ammonia concentrations. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that blood and CSF ammonia concentrations in dogs with EHPSS were greater than those for healthy dogs and were strongly and positively correlated, albeit in a nonlinear manner. This suggested that the permeability of the blood-brain barrier to ammonia may be abnormally increased in dogs with EHPSS, but further investigation of the relationship between blood or CSF ammonia concentration and clinical signs of hepatic encephalopathy or the surgical outcome for dogs with EHPSS is warranted.

Helicobacter pylori infection among patients with liver cirrhosis

Background and aimInflammatory changes in the stomach caused by Helicobacter pylori indirectly and directly affect liver function. Moreover, the bacteria may worsen the course of the liver cirrhosis. The study aimed at evaluating the incidence of H. pylori infection among patients with liver cirrhosis, depending on the etiology and injury stage, scored according to Child–Pugh classification. Stage of esophageal varices and endoscopic inflammatory lesions in the stomach were evaluated, depending on the presence of H. pylori infection.Patients and methodsThe study included 147 patients with liver cirrhosis: 42 were infected with hepatitis C virus, 31 were infected with hepatitis B virus, 56 had alcoholic liver cirrhosis, and 18 had primary biliary cirrhosis. Diagnosis of H. pylori infection was performed based on the presence of immunoglobulin G antibodies in serum.ResultsH. pylori infection was found in 46.9% of patients. The incidence of H. pylori infection among patients with postinflammatory liver cirrhosis was significantly higher (P=0.001), as compared with patients with alcoholic liver cirrhosis. Ammonia concentration was significantly higher in patients infected with H. pylori, compared with noninfected individuals (129 vs. 112 μmol/l; P=0.002). Incidence of H. pylori infection in patients without esophageal varices was significantly lower compared with patients with esophageal varices (14 vs. 60%; P<0.001).ConclusionH. pylori infection is significantly more frequent among patients with postinflammatory liver cirrhosis (infected with hepatitis C virus or hepatitis B virus) than in patients with alcoholic liver cirrhosis or primary biliary cirrhosis. H. pylori infection correlates with elevated concentration of blood ammonia and the incidence of esophageal varices.