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)

The effect of adrenaline on acetylcholine synthesis, choline acetylase and cholinesterase activity. Acta Physiol. Pol. 1975, 26 (1): 45-54. The purpose of the study was to assess the participation of adrenaline in the processes of acetylcholine synthesis and breakdown in white rats. After intraperitoneal administration of adrenaline the content of acetylcholine in the tissues (brain, stomach, sciatic nerve, lumbar spinal cord) initially, slightly decreased, increased in the 30th, 60th, and 120th min, and then fell again below the initial value after 240 min. The rise in acetylcholine tissue content after administration of adrenaline seems to be due to its increased synthesis. This was also confirmed by in vitro investigations. The fall in the tissue acetylcholine content was associated with reduced synthesis of acetylcholine in the cerebral cortex. The increase in acetylcholine synthesis in the brain tissue after adrenaline given in vitro and in vivo does not seem to be caused by activation of choline acetylase. The activity of cholinesterase in the brain was not changed after adrenaline administered in vivo and in vitro.
Acta Physiol Pol
PMID:The effect of adrenaline on acetylcholine synthesis, choline acetylase and cholinesterase activity. 12 24

In Huntington's chorea the biochemical disturbances are to some degree a reverse of those observed in Parkinson's disease and a failure of the cholinergic system is prevalent. Former attempts at treatment were based on blockade of the dopaminergic system. The author suggests that the general line of treatment should be -- similarly as in Parkinson's disease -- not blockade of the predominant system but enhancing the cholinergic activity by administration of acetylcholine precursors and agents blocking cholinesterase. Eight patients were treated in this way and significant improvement was achieved in half of them. Further therapeutic trials along these lines are justified theoretically and the main problem will be to find substances crossing the blood-brain barrier and acting more strongly.
Neurol Neurochir Pol
PMID:[New attempt at treating Huntington's chorea (preliminary report)]. 13 May 61

Hyperkineses are a clinical and pathogenetic counter-part of parkinsonism (MP). Their underlying cause is increased activity of the dopaminergic system or insufficiency of the cholinergic system. Treatment inhibiting the dopaminergic system, similarly as anticholinergic treatment is of little effectiveness in MP. A trial of substitutive treatment was undertaken activating the cholinergic system with a precursor of acetylcholine (dimethyl-amino-ethanol-deanol--Bimanol) with simultaneous inhibition of cholinesterase with prostigmin. The results of this treatment were compared with previously applied antidopaminergic treatment (Haloperidol) and with the effects of L-dopa. This treatment was given to 11 patients with Huntington's chorea (ChH), 4 with faciolingual dyskinesis (DFL), 3 with torticollis spasmodicus (TS), 3 with maladie des tics (MT) and 8 with dyskinesia following treatment with L-dopa (MP). Cholinergizing treatment gave better results than antidopaminergic treatment in TS and ChH, and worse in MT. In dyskinesia following L-dopa cholinergizing treatment gave also no effects reported by others. Differences in the results of cholinergizing and antidopaminergic treatment may indicate non-homogenous pathological mechanism of these hyperkineses. Cholinergizing treatment in hyperkineses is based on a similar principle as L-dopa treatment in MP and this approach seems to be proper but more effective preparations should be sought for.
Neurol Neurochir Pol
PMID:[Cholinergizing treatment in hyperkinesis]. 15 May 48

Gamma-aminobutyric acid, 0.6, 0.8 and 1.6 mg/rat, ivc, increased the level of acetylcholine (ACh) in the striatum, and in doses 0.2-1.6 mg/rat ivc, accelerated synthesis of ACh. The former effect commenced 5 min. after the injection, reached its peak 15 min. and declined after 30 min. The ACh synthesis increased 15 and 30 min. after the injection and declined after 60 and 120 min. Gamma-aminobutyric acid increased the activity of choline acetyltransferase but did not affect activity of choline esterase.
Pol J Pharmacol Pharm
PMID:The effect of gamma-aminobutyric acid on the content and metabolism of acetylcholine in the rat striatum. 54 77

An electrochemical method was elaborated for the continuous determination of enzymatic hydrolysis of acetylcholine. In the electrochemical system applied the aqueous solution of the enzyme is separated from the aqueous solutions of substrates by a semipermeable membrane. In this way cholinesterase is used many times for reactions. Changes in the concentration of hydrogen ions were determined with molybdenum electrodes, one of which was used as an indicator and immersed in enzyme solution and the other served for comparison and was immersed in the solution of acetylcholine flowing to the measuring system.
Acta Physiol Pol
PMID:Electrochemical method for continuous determination of enzymatic acetylocholine hydrolysis. 59 97

The effect of reserpine on acetylcholine synthesis, choline acetylase and cholinesterase activity. Acta Physiol. Pol. 1975, 26 (1): 55-61. Reserpine-induced changes in ACh content in various tissues of white rats (cerebral cortex and brain stem, stomach, lungs, heart, spleen) and the effects of reserpine on the synthesis, enzymatic breakdown of ACh, and ChAc activity were studied. Reserpine administered subcutaneously caused a singificant rise in ACh content of the cerebral cortex and insignificant rise in the heart and spleen. Reserpine (in a concentration of 0.25 mug/ml) had no effect on ACh synthesis in vitro. Reserpine in vivo increased significantly ACh synthesis in the brain. No effect of reserpine on ChAc and AChE activity was demonstrated.
Acta Physiol Pol
PMID:The effect of reserpine on acetylcholine synthesis, choline acetylase and cholinesterase activity. 113 Feb 19

In 50 patients with mitral stenosis in the stage of maximal clinical improvement a correlation between the functional state of liver and the morphological changes was estblished. For this purpose the serum total bilirubin concentration was determined together with the serum total protein, albumin and globulin levels, serum alanine aminotransferase, aspartate aminotransferase, cholinesterase, leucylaminopeptidase, and alkaline phosphatase activities. The bromsulphalein test, provoked hypoprothrombinemia test, and histological examination of liver biopsy specimens were made. It was found that with increasing liver morphological lesions there is a gradual but not parallel impairment of function. The most sensitive index of hepatic functional disturbances was the test of provoked hypoprothrombinemia according to Kirchmayer and Bromowiczowa. For full assessment of the degree to which the changes in the congested liver have advanced it is necessary to perform liver function tests in combination with histological examination of the organ.
Pol Med Sci Hist Bull
PMID:Correlation of liver function and morphological abnormalities in mitral stenosis. 122 31

Research was conducted upon 28 patients with a diagnosis of endogenous depression after their pharmacological treatment with imipramine or chlorimipramine. The investigation considered the interrelationship between psychophysiological parameters (heart rate, respiration rhythm, postural muscular tension) and the indices of the cholinergic and adrenergic systems (kinetic parameters of choline transport in the blood; Vmax, the activity of plasmic pseudocholinesterase, Che; blood acetylcholinesterase AChE, monoaminoxidase in blood platelets, MAO; and dopamine beta hydroxylase DBH). The results indicate that during relapse of endogenous depression there occurs an imbalance in the cholinergic-adrenergic systems which may be the result of some somatic symptoms typically found in the depression syndrome. The appearance, after pharmacotherapy, of a correlation between the indices of the activity of the cholinergic system with the respiratory rhythm suggest that the part played by the cholinergic mechanism in the regulation of autonomic processes normalizes itself during the course of successful therapy. The appearance of characteristic correlations between the activity of the cholinergic and adrenergic systems and the psychophysiological parameters in the presence of relatively low psychological stress seems to accompany successful treatment with imipramine and chlorimipramine.
Psychiatr Pol
PMID:[Psychophysiological characteristics and metabolic indices of neurotransmitter metabolism in patients ill with endogenous depression]. 130 98

The effects of single i.p. injections of two cholinesterase inhibitors, chlorphenvinphos (CVP) and physostigmine, on hippocampal and cortical EEG and flash evoked potentials in occipital cortex were compared in rabbits and rats. A comprised method of spectral analysis was employed for evaluation of changes in EEG. The obtained results showed that in both species the changes in hippocampal and cortical EEG after administration of CVP were relatively small or negligible in comparison with those after physostigmine administered in doses resulting in comparable (or even lesser) inhibition of blood cholinesterase (ChE). Neither CVP nor physostigmine resulted in significant changes in the morphology of the flash evoked potentials. The data do not confirm the suggestion that brain electrical activity is the most sensitive index of neurotoxicity resulting from exposure to organophosphate ChE inhibitors.
Pol J Occup Med Environ Health 1992
PMID:A comparison of changes in spontaneous (EEG) and evoked brain activity induced by chlorphenvinphos and physostigmine in rats and rabbits. 139 53

A case of prolonged QT syndrome (PQTS) caused by unintentional poisoning with organic phosphate pesticides is reported in a 73 year old farmer. PQTS developed and coexisted with other symptoms of poisoning such as low levels of cholinesterase, vomitus, diarrhoea, miosis, hypersalivation and occurred with typical symptoms. Despite concomitant with PQTS advanced ventricular extrasystoles the most dangerous form of them--ventricular tachycardia "torsades de pointes"--wasn't observed what was attributed among other things to scrupulous control and replenishment of potassium++ and magnesium and avoidance of typical antiarhytmic drugs in ventricular arrhythmia+ treatment. Acquired (most often after drug treatment, toxic and resulting from electrolytic disturbances) forms of PQTS are discussed stressing their heterogeneity and necessity of preventive treatment (different, dependent on etiology).
Kardiol Pol 1992 Apr
PMID:[Long QT syndrome after organophosphate insecticide poisoning]. 164 Jun 67


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