Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Three groups of 200-gm rats were injected subcutaneously with neostigmine methylsulfate (1 mg/kg/day) for 7, 30, and 100 days. Electrophysiological changes were assessed in vitro, using microelectrode techniques to examine diaphragm muscles of treated and untreated animals. Miniature end-plate potential (MEPP) amplitude decreased in neostigmine-treated preparations. Guanidine hydrochloride enhances transmitter release and increases MEPP frequency in control preparations. Neostigmine-treated animals examined between 6 to 72 hours after discontinuation of neostigmine therapy showed impaired response to the facilitating influence of guanidine. Recovery of response to guanidine was inversely related to length of treatment with neostigmine. Results of electron-microscopic examination of motor end-plates in treated animals revealed ultrastructural changes, including simplified end-plates, and, occasionally, multiple, separate, junctional regions. Therefore, the chronic administration of cholinesterase inhibitors in man may have a deleterious effect, as well as a transient beneficial one.
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PMID:Neostigmine methylsulfate. Does it have a chronic effect as well as a transient one? 17 68

After discussion of the modern concepts of pathophysiology of ocular myasthenia the ocular symptoms such as ptosis and eye muscle palsies are discussed. As important diagnostic sign the Simpson lid fatigue test before and after application of Tensilon is described. For diagnosis of myasthenic eye muscle palsies electrooculography has a special significance especially in connection with the application of Edrophonium, which normalizes myasthenic hypometric saccades and transforms them even in hypermetric saccades. In doubtful cases of eye muscle palsies the electromyogram of the affected muscle in connection with the Edrophonium-test is extremely valuable. With regard to modern treatment apart from cholinesterase inhibitors (Pyridostigmine, Neostigmine) thymectomy, the application of corticosteroids, ACTH and especially also immune suppressive drugs (Imurel etc.) is discussed. Of great significance in ocular myasthenia is the local application of cholinesterase inhibitors like Eserine, Prostigmin or Phospholine Iodide.
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PMID:[Diagnosis and treatment of ocular myasthenia (author's transl)]. 20 42

1. The cholinesterase inhibitors neostigmine, edrophonium and eserine (7 x 10(-7) M) reduced m.e.p.p. frequency by some 50% at the frog neuromuscular junction. Neostigmine also produced a small reduction in quantal content. 2. Tetraisopropylpyrophosphoramide, with a high specificity for non-specific cholinesterase, has a similar effect on m.e.p.p. frequency but ambenonium, with a high specificity for acetylcholinesterase, was markedly less effective in this respect. 3. Carbachol (10(-5) M) and the muscarinic agonists muscarine and metacholine (7 x 10(-7) M) also reduced the rate of spontaneous release. 4. The action of neostigmine was antagonized by atropine, but not by D-tubocurarine. Muscarine did not have any further effect when m.e.p.p. frequency was reduced with neostigmine. 5. Experiments with reduced extracellular Ca2+ concentration suggest that the cholinergic agents reduce Ca2+ permeability directly at the presynaptic terminals and that they do not act via a change in PNa or PK. It is suggested that the consequent reduction in Ca2+ entry causes a fall in both evoked release and in intracellular Ca2+ concentration, thereby reducing m.e.p.p. frequency. 6. It is concluded that non-specific cholinesterases present on the presynaptic terminals can act as inhibitory muscarinic cholinergic receptors. This form of presynaptic inhibition at the amphibian neuromuscular junction contrasts with that described in the mammalian preparation in which the sites are blocked by D-tubocurarine and are excitatory.
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PMID:Inhibitory effects of cholinergic agents on the release of transmitter at the frog neuromuscular junction. 22 16

Ninety-three patients 65 years of age or older were studied to determine the incidence of dysrhymia following administration of 1 of 2 cholinesterase inhibitors, neostigmine or pyridostigmine. The ECG was then continuously monitored for 90 minutes. Neostigmine was associated with a higher incidence of dysrhythmia than was pyridostigmine. Neostigmine administered to patients with pre-existing coronary artery disease and/or conduction defects and to patients with hypertension was associated with a significantly higher incidence of dysrhythmia than was pyridostigmine when administered to patients with the same conditions. The incidence of dysrhythmia in patients who received a halogenated anesthetic was 5 times greater after neostigmine than after pyridostigmine.
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PMID:Cardiac dysrhythmia following reversal of neuromuscular blocking agents in geriatric patients. 56 56

Hypothalamic neuronal activities of noradrenaline, dopamine and serotonin as well as serum glucose concentrations were simultaneously monitored 60 min after the third cerebroventricular injection of neostigmine, a cholinesterase inhibitor, in rats. Each neuronal activity was assessed from a ratio of the concentration of the major metabolite to that of its precursor monoamine itself by using the technique of gas chromatography-mass spectrometry. Neostigmine caused significant increases in serum glucose concentrations, hypothalamic noradrenergic and dopaminergic neuronal activities, and significantly suppressed hypothalamic serotonergic neuronal activity. All these responses to neostigmine were completely inhibited by the co-administration of atropine. These observations emphasize the important role of the interactions between cholinergic (muscarinic) and monoaminergic neurons in the brain.
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PMID:Effects of intracerebroventricularly administered neostigmine on hypothalamic monoaminergic neuronal activities in awake rats. 138 54

Twenty anephric and 20 healthy patients received a bolus dose of mivacurium 150 micrograms kg-1. When the first EMG response (T1) of the train-of-four had recovered to 5% of control (T0), an infusion of mivacurium 10 micrograms kg-1 min-1 was started and adjusted to keep T1 at 5%. Ten patients in each group were given neostigmine 35 micrograms kg-1 when the infusion was stopped when T1/T0 had recovered to 20%; in the others recovery was spontaneous. After the bolus dose of mivacurium, mean (SD) depression of T1 was greater in the anephric group than in the normal group (98.4 (3.5) vs 96.8 (4.4)%; P less than 0.01) and recovery of T1/T0 to 5% was slower (15.3 (6.9) vs 9.8 (3.5) min; P less than 0.01). Anephric patients required a slower infusion rate (6.3 (1.9) vs 10.4 (2.8) micrograms kg-1 min-1; P less than 0.001). Neostigmine hastened recovery of both T1/T0 and T4/T1 in both groups. Spontaneous recovery of T1/T0 (from 25% to 75%) after the infusion was also slower in anephric patients (12.2 (8.2) vs 7.7 (1.2) min; P less than 0.05). Plasma cholinesterase activity was less in the anephric group (785 (207) vs 943 (217) iu litre-1; P less than 0.05) and there was a (negative) correlation overall between cholinesterase activity and time to 5% recovery of T1/T0 after the bolus dose (r = -0.42; P less than 0.02). We conclude that patients with chronic renal failure may require a reduced dose of mivacurium.
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PMID:Use of mivacurium chloride by constant infusion in the anephric patient. 164 38

A patient with severe organophosphate intoxication received Neostigmine 1 mg IV during the intermediate syndrome. This dose resulted clinically and neurophysiologically in a marked deterioration of neuro-muscular transmission. This effect of neostigmine on the neuromuscular block during the intermediate syndrome (deterioration) differs from its effect on a similar pattern (improvement), which is seen in the delayed neuropathy following organophosphate exposure. The administration of therapeutic doses of cholinesterase inhibitors in patients with a reduced safety margin due to inhibition of endplate acetylcholinesterase may be dangerous.
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PMID:[The effect of neostigmine on the motor endplate in the intermediate syndrome of organophosphate poisoning]. 165 Jun 95

Acetylcholinesterase inhibitors produce diverse physiologic effects, but lethal exposure consistently produces respiratory failure due to neuromuscular paralysis or depression of respiratory control centers in the medulla. Simultaneous measurement of gastrocnemius muscle contraction and efferent phrenic nerve activity was used to determine the primary cause of respiratory failure produced by neostigmine and diisopropyl fluorophosphate (DFP) in anesthetized cats. Both neostigmine and DFP abolished phrenic nerve activity prior to producing neuromuscular blockade. Furthermore, neostigmine did not alter brain acetylcholinesterase activity and pretreatment with either atropine methylbromide or atropine increased the dose of neostigmine required to abolish phrenic nerve activity. In contrast, DFP abolished brain cholinesterase activity and only atropine inhibited its respiratory effects. Despite the loss of efferent phrenic nerve activity, there is no evidence of a direct effect of neostigmine on respiratory control centers. Neostigmine may instead alter afferent inputs which modulate respiration to produce a reflex respiratory failure.
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PMID:Mechanisms of respiratory failure produced by neostigmine and diisopropyl fluorophosphate. 206 14

In order to investigate the correlation between the peripheral ACh and the primary input of acupuncture sensation, in the paper the cholinesterase inhibitor--Neostigmine and the ACh synthesis blocker--Hemicholine, which are unable to pass through blood brain barrier, and ACh were used as tools to increase or decrease the level of ACh in peripheral nerve system of rats. The results indicated that: 1) The effect of electroacupuncture analgesia can be enhanced by subcutaneous injection of neostigmine which related to the dosage used. 2) The influence of electroacupuncture analgesia can be markedly inhibited by intraperitoneal injection of Hemicholine. 3) This influence of suppression by Hemicholine can be reversed at once when acetylcholine in combination with neostigmine was injected. But could not reverse by neostigmine alone. It suggested that the effect of electroacupuncture analgesia and the primary input of acupuncture sensation were significantly related to the level and content of ACh in periphery.
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PMID:[Acetylcholine and the primary input of acupuncture sensation--influence of peripheral acetylcholine on the role of electroacupuncture analgesia]. 212 63

This study investigated the relationship between central cholinergic neurons and insulin secretion in bilateral adrenalectomized fed rats. Neostigmine (a cholinesterase inhibitor, 5 x 10(-8) mol) administered into the third cerebral ventricle produced significant increases in hepatic venous plasma insulin and glucose concentrations, whereas i.v. injection of the same dose of neostigmine did not. Prior acute subdiaphragmatic vagotomy or i.p. pre-injection with methylatropine (10(-8) mol) completely prevented the neostigmine-induced rise in plasma insulin concentration. Intraperitoneal pretreatment with hexamethonium (5 x 10(-8) mol) also significantly reduced the plasma insulin response. These peripheral pretreatments did not change the plasma glucose response to neostigmine. Intraventricular co-administration of 10(-9) mol methylatropine, a dose that was ineffective when pre-injected i.p., eliminated the plasma insulin and glucose responses to neostigmine, whereas hexamethonium (5 x 10(-8) mol) had no influence on either response to neostigmine. These observations suggest that stimulation of central cholinergic-muscarinic neurons with third cerebral ventricular injection of neostigmine results in vagally mediated insulin secretion in bilateral adrenalectomized fed rats.
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PMID:Vagally mediated insulin secretion by stimulation of brain cholinergic neurons with neostigmine in bilateral adrenalectomized rats. 257 Jun 20


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