Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

EEG studies were done in 19 patients comatose due to severe hepatic insufficiency associated with porto-caval shunting. The neurological deficits were graded in 5 stages and related to the abnormal EEG-pattern observed in 38 records. With deepening of coma, alpha-frequencies were gradually replaced by theta- and delta-activities. The frequency of theta- and delta-runs decreased with neurological deterioration. Triphasic waves (typical and/or atypical) were seen in 26% of the records. Typical triphasic waves were found to be limited to stage 3 of coma, whereas atypical forms appeared in earlier and later stages. After infusions of L-Valin, a transient improvement and disappearance of triphasic waves was observed, but no significant effect could be established on the final course of the disease. Sleep-like potentials and the reactivity to external stimuli decreased in deep stages of coma. Severe EEG abnormalities were correlated to low cholinesterase and high lactid acid blood level, but no correlation was found to the level of ammonia.
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PMID:[Electroencephalographic changes in coma due to hepatic insufficiency with porto-caval shunt (author's transl)]. 11

In 75 cases of histologically verified liver cirrhosis the plasma amino acids were determined by ion exchange chromatography and the results were correlated with different liver function tests as prothrombin time, pseudocholinesterase, serum albumin, GOT, bilirubin and venous ammonia. Out of these parameters prothrombin time, pseudocholinesterase and serum albumin significantly correlated with the sum of branched-chain amino acids and with the Fischer's quotient (molar ratio of branched-chain and aromatic amino acids). Methionin and aromatic amino acids inversely correlated with these parameters, additionally methionin positively correlated with bilirubin and GOT. By comparing plasma amino acid levels in cirrhotics without and with hepatic encephalopathy (grade 3 or 4) no significant differences were found. "Fischer's quotient" showed an overlap in patients with and without encephalopathy. Therefore the precipitation of hepatic encephalopathy is not fully explained by the changes in plasma amino acids. Therapeutic administrations of specially mixtures of amino acids with a high content in branched-chain and a low content in aromatic amino acids correct the plasma amino inbalance for a short time and improves hepatic encephalopathy.
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PMID:Plasma amino acids in hepatic encephalopathy. 29 Jul 44

The influence of meat containing ammonia in concentrations of 0.1 and 0.3% was studied in chronic experiments on 3 generations of rats (males and females). To investigate the function of the liver, kidneys and CNS, alanine-aminotransferase, lactate dehydrogenase activity, and the content of the total protein and its fractions were assayed in the blood serum; cholinesterase activity, sulfhydryl groups, urea and residual nitrogen were assayed in the blood, as well as the parameters of rheobase, chronaxie and summation of subliminal impulses. The results of the investigation have shown that meat containing ammonia in concentrations of 0.1 and 0.3% produces a detrimental effect on the experimental animals, the highest effect being recorded with an ammonia concentration of 0.3%.
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PMID:[Study of the possible harmful action of meat containing ammonia on experimental animals]. 260 59

Monocularly deprived (MD) cats show a loss of responsiveness to visual stimulation of the deprived eye among visual cortical neurons. Several lines of evidence suggest that this effect involves, at least in part, a suppression of deprived eye input, possibly mediated by GABA inhibition. In order to better understand the nature of this suppression we have evaluated the effectiveness of different types of disinhibitory and excitatory agents to reverse the effects of MD. We investigated bicuculline (a GABA antagonist); picrotoxin (a GABA antagonist with a different mechanism of action from bicuculline); strychnine (a glycine antagonist); ammonium ion (a blocker of membrane chloride channels); physostigmine (a cholinesterase inhibitor); and naloxone (an opiate antagonist and also a GABA antagonist). All drugs were given intravenously. Bicuculline restored binocularity to 50% of the visual cortical neurons tested and naloxone to 36%. With both drugs, receptive fields of the normal eye tended to lose specificity. The emergent deprived eye receptive fields were usually similar to those of the normal eye after drug administration. Ammonium ion produced binocular responses in 27% of neurons tested, but receptive fields were grossly abnormal; moreover, ammonium infusion tended to depress neuronal responsiveness. All other drugs tested failed to restore binocularity. These experiments lend further credence to the hypothesis that GABA inhibition contributes to the cortical effects of MD, since only drugs with GABA antagonistic action were effective in restoring neuronal responsiveness to the deprived eye.
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PMID:Comparative pharmacological effects on visual cortical neurons in monocularly deprived cats. 299 1

Studies have been made of the effect of three groups of ammonia reversible inhibitors on the activity of erythrocyte acetylcholinesterase, serum butyrylcholinesterase, cholinesterase from frog brain, as well as cholinesterases from the optical ganglia of the Pacific and three populations of the commander squids. Determination of kinetic parameters of the reversible inhibition of these enzymes revealed differences resulting from the specific structure of their catalytic centers. Tetramethylammonium assay confirmed different properties of cholinesterases in individuals of the commander squid from various habitats in the Bering Sea; this finding may be taken as an indication of intraspecific differentiation of these cephalopods. Certain similarity was noted in the inhibitory specificity of cholinesterases from the Pacific and "southern" commander squids with the overlapping habitats.
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PMID:[The specificity of the interaction of the cholinesterases in Far Eastern squid and certain vertebrates with reversible inhibitors]. 326 46

Alcohol, hepatitis B, and Non A Non B hepatitis were the main aetiologies of 124 patients with hepatic encephalopathy (HE) due to histologically proven liver cirrhosis. All had severe portal hypertension (PH) and usually increased inflammatory activity of the liver. In stage I (n = 27) 7.4% died, in stage II (n = 28) 14.3%, in stage III (n = 32) 50% and in stage IV (n = 37) 94.6%. Even in cirrhotics without PH, serum albumin, cholinesterase activity and prothrombin time (PT) were significantly decreased. But only in the case of PT did the magnitude of the decrease parallel the stage of HE. Hyperammonaemia and serum creatinine were increased in parallel with the stage of HE. Therefore, in liver cirrhosis a quotient derived from decreased PT and increased serum creatinine has a good prognostic value. Early diagnosis of HE is possible on the basis of writing tests and the determination of free or toxic ammonia.
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PMID:The role of protein metabolism in 204 liver cirrhotics with and without hepatic encephalopathy. I. Clinical and general biochemical findings. 372 88

Healthy camels were experimentally infected with Trypanosoma evansi and then treated with isometamidium chloride (samorin) at single intravenous doses of 0.5 or 1.0 mg/kg. Five to 10 min after the drug administration, the camels at both dosages showed lacrimation, salivation, trembling, restlessness, frequent urination and defecation, followed by diarrhea. Moreover, the camels at the higher dose showed an unsteady gait for about an hour with hindleg weakness and walking backward. The animals fell to the ground, laid on their sides, and bent their necks into an "S" shaped curve. Three hours after the drug administration all the animals stood up and remained quiet. The treatment increased the concentration of plasma ammonia and total protein. No significant change was found in the plasma bilirubin concentration. Two hours after treatment, the activity of plasma cholinesterase was significantly reduced. The enzyme activity recovered 24 h after drug administration, but was still significantly below the control value. The treatment did not produce statistically significant changes in the hemogram of the infected camels. The results suggest that the drug should not be used clinically against T evansi infection due to its low margin of safety. If the drug is to be used at all in camels, pretreatment with an anticholinergic agent might be considered.
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PMID:Some observations on the toxicosis of isometamidium chloride (samorin) in camels. 377 85

Short- and long-term ammonia toxicity was induced in mice by intraperitoneal injection, respectively, of single and six doses of 0.6 mM ammonium acetate per 100 g of body weight. The animals were sacrificed half an hour after either the single injection or after the last injection of six doses. Under these experimental conditions the ammonia levels were found to be elevated twofold in cerebral cortex, brain stem, and basal ganglia after the administration of a single dose of ammonium acetate. A fourfold increase in the content of ammonia was observed in cerebral cortex, brain stem, and basal ganglia after six injections. An elevation in the activity of pseudocholinesterase (enzyme localized in brain capillaries and glial cells) in all the above four regions resulted as a short-term effect of ammonia toxicity. True acetylcholinesterase was found to be elevated in all the four regions in short-term and in long-term ammonia toxicity. Gamma-glutamyltranspeptidase (GGTP), another enzyme localized in cerebral capillaries and glial cells, was found to be depressed in all the regions of the brain in both short- and long-term ammonia toxicity. The implications of these results are discussed in relation to glial cell function.
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PMID:Studies on acetylcholinesterase and gamma-glutamyltranspeptidase in mouse brain in ammonia toxicity. 613 7

Studied were 12 cows with protracted, recurrent acidosis of the rumen, 4 cows with alkalosis, and 2 calves with experimental acidosis, following up the changes in the rumen content and their impact on the liver. The diseased animals were investigated both clinically and by laboratory tests with regard to alkaline phosphatase, plasma cholinesterase, SGOT, SGPT, alkali reserves, bilirubin, blood sugar, protein function of the liver (flocculation tests), biopsy of the liver, urine pH, urobilinogen, sedimentation test and ketone bodies, rumen pH, rumen infusoria, glucose-fermenting and cellulose-digesting activity, breakdown of nitrates, butyric acid, and ammonia gas. It was found that recurrent physiologic deviations of the rumen content play an essential pathogenetic role in liver injury. The more substantial and continuous the deviations the more severe the liver diseases. Studies revealed that along with other factors the recurrent acidosis and alkalosis of the rumen content could be claimed to be an immediate cause of the liver diseases in high producing cows. Histologically, the liver of cows with slightly expressed acidosis of the rumen showed granular degeneration, and of cows with protracted acidosis--fatty degeneration, activation of the reticulo-endothelial system, and leukocytes in the capillar sinusoids. Liver biopsy in the case of experimental acidosis demonstrated also decrease in the glycogen content of the hepatocytes.
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PMID:[Liver diseases and their relationship to forestomach function in highly productive cows]. 734 34

Glucose intolerance and diabetes mellitus are both prevalent in patients with chronic liver diseases. We examined the efficacy and systemic safety of therapy with an alpha-glucosidase inhibitor, acarbose, in diabetes mellitus associated with chronic liver diseases. Twenty patients with chronic hepatitis or liver cirrhosis and overt diabetes mellitus received acarbose (taken orally) for 8 weeks. The initial dosage of acarbose was 50 mg three times daily, taken before meals; this was increased to 100 mg three times daily after 2 weeks. The mean fasting plasma glucose level was 173.7 +/- 18.6 mg/dl (mean +/- SE) at entry, and was significantly decreased to 132.9 +/- 7.5 mg/dl (P < 0.05) after 8 weeks of acarbose treatment. The improved glycemic control was reflected by a significant decrease in glycosylated hemoglobin (HbA1c) from 7.2 +/- 0.3% at entry to 6.3 +/- 0.2% (P < 0.05) after 8 weeks. Serum levels of both aspartate and alanine aminotransferases fluctuated during acarbose treatment, probably due to the natural course of chronic liver diseases, but the mean values had decreased after 8 weeks of treatment. Plasma ammonia levels increased, from 61.3 +/- 10.7 micrograms/dl to 71.1 +/- 9.6 micrograms/dl after 8 weeks of acarbose treatment but the increase was not significant. Clinically significant elevation of plasma ammonia concentration was seen in 2 cirrhotic patients (121 and 124 micrograms/dl); this was asymptomatic and gradually returned to the normal range despite continuous acarbose treatment in one patient, and was reversed after the withdrawal of acarbose with the concomitant administration of lactulose in the other patient. No other blood tests results, including albumin, cholinesterase, and prothrombin time, or lipid profile and nutritional status, in terms of rapid turnover proteins, prealbumin, retinol binding protein, and transferin, were altered throughout the study period. These results indicate that diabetes mellitus associated with chronic liver diseases may be safely and effectively treated with acarbose. However, clinicians must be aware of the possibility of hyperammonemia when they prescribe acarbose for patients with diabetes mellitus and advanced liver cirrhosis.
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PMID:Safe and effective treatment of diabetes mellitus associated with chronic liver diseases with an alpha-glucosidase inhibitor, acarbose. 943 16


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