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PubMed1966

INTRODUCTION

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Adolescent↗
PubMed1971

The synthesis, turnover and release of surplus acetylcholine in a sympathetic ganglion.

1. Surplus acetylcholine (ACh) is the extra ACh that accumulates in cholinergic nerve endings when they are exposed to an anticholinesterase agent. The synthesis and turnover of this ACh was examined in the cat's superior cervical ganglion.2. Surplus ACh did not accumulate in chronically decentralized ganglia perfused with eserine-choline-Locke solution, and this shows that it is stored in presynaptic nerve terminals.3. Surplus ACh accumulated more rapidly in ganglia perfused with eserine than in ganglia perfused with neostigmine or with ambenonium; accumulation was delayed by 45-60 min when a quaternary anticholinesterase was used. However, the release of ACh upon preganglionic nerve stimulation was the same during perfusion with eserine, neostigmine or ambenonium. It is concluded that intracellular acetylcholinesterase normally destroys surplus ACh, whereas extracellular enzyme destroys released ACh.4. When ganglia were perfused with [(3)H]choline and eserine, the surplus ACh that accumulated was labelled but its specific radioactivity was only 38% of that of the choline added to the perfusion fluid.5. Surplus ACh was not released by nerve stimulation and was not mobilized for release during, or after, prolonged nerve stimulation. It is concluded that ACh released by nerve impulses is replaced by synthesis at the site of ACh storage and not by movement of ACh from the surplus pool.6. The accumulation of surplus ACh no more than doubled the total ACh content of ganglia, but turnover of ACh continued when the total amount was constant. Surplus ACh may contribute to spontaneous ACh output from eserinized preparations.7. When ganglia were perfused with a medium containing high K(+) (56 mM), surplus ACh was released.

Acetylcholine↗
PubMed2000

Coronary spastic angina induced by anticholinesterase medication for myasthenia gravis--a case report.

Myasthenia gravis (MG) is characterized by weakness of skeletal muscles because of a decrease in the number of available acetylcholine receptors at neuromuscular junctions. Anticholinesterase medication is widely used to treat MG, but muscarinic side effects sometimes appear and limit the drug usage. To their knowledge, the authors present the first case of coronary spastic angina quite possibly induced by anticholinesterase medication to treat MG. The appearance of coronary spastic angina in the present case is likely mediated through the increase of acethylcholine by anticholinesterase medication.

Aged↗
PubMed1977

Myasthenia gravis and Schmidt syndrome.

A patient with myasthenia gravis developed both Addison disease and primary hypothyroidism, with demonstrable anti-adrenal and antithyroid antibodies in her serum. The association of myasthenia gravis with Schmidt syndrome does not seem to be a chance occurrence, considering the autoimmune pathogenesis of each of these disorders.

Addison Disease↗
PubMed1993

Sensitive determination of ambenonium in plasma using inhibitory activity to acetylcholinesterase.

A sensitive analytical method for the determination of ambenonium, a selective acetylcholinesterase inhibitor, in plasma was developed. The procedure involves ultrafiltration to remove endogenous plasma cholinesterase, followed by colorimetric measurement of the inhibitory activity to acetylcholinesterase by the thiocholine method. Coefficient of variation of within-day triplicate analysis is less than 20% at the concentration of 5 nM. Detection limit of this method is 1 nM, which is twice lower than the most sensitive HPLC method reported previously. This assay procedure is applied to the pharmacokinetic study of ambenonium after intravenous administration of low dose (10-20 nmol/kg) to rat. This new method is rapid and simple and makes it possible to determine the ambenonium concentration in plasma with good accuracy.

Acetylcholinesterase↗
PubMed1994

Appearance of tolerance in the increase of contractile muscle tension by ambenonium in rats.

The relationship between the concentration of ambenonium (AMB), a selective and reversible acetylcholinesterase (AChE) inhibitor, in plasma and the potentiation of contractile muscle tension was investigated using a sciatic nerve-muscle preparation of rat. The developed isometric contraction was enhanced dose-dependently after i.v. administration of low doses (5-20 nmol/kg) of AMB, but the contraction was weakened when AMB was administered at high doses (100-1000 nmol/kg), and the concentration-effect relationship was bell-shaped. The muscle contraction profile after 50 nmol/kg administration without previous administration, with 20 nmol/kg and with 50 nmol/kg administered previously were quite different from each other. These findings suggest that the potentiation of contractile muscle tension by AMB may be acutely tolerated and the concentration-effect relationship may change time-dependently.

Ambenonium Chloride↗
PubMed1995

Comparative pharmacokinetics of four cholinesterase inhibitors in rats.

Pharmacokinetics of a very short-acting, a short-acting and two long-acting cholinesterase (ChE) inhibitors, edrophonium, neostigmine, pyridostigmine and ambenonium, respectively, were compared to elucidate the major determinant of their pharmacokinetics. No dose-dependency in pharmacokinetic behavior was observed within the range of 2-10 mumol/kg for edrophonium, 0.5-2 mumol/kg for pyridostigmine, 0.1-0.5 mumol/kg for neostigmine and 0.3-3 mumol/kg for ambenonium, respectively. Neostigmine has the shortest elimination half-life, and edrophonium, pyridostigmine and ambenonium follow in that. Four ChE inhibitors have similar Vdss values within the range of 0.3-0.7 l/kg, which is similar to the muscle/plasma concentration ratio of these drugs. The liver or kidney to plasma concentration ratio of all ChE inhibitors at 20min after i.v. administration ranged from 5 to 15. Small distribution volumes estimated from the plasma concentration profiles may reflect the distribution to muscle and to the extracellular space of other organs/tissues, while the rapid disappearance of ChE inhibitors from plasma may reflect the concentrative uptake to the liver and kidney.

Ambenonium Chloride↗
PubMed1976

[Interaction of reversible inhibitors with the catalytic centers and allosteric sites of cholinesterases].

The kinetics of inhibition of the human red blood cell cholinesterase with galanthamine tacrine and oxazyl (ambenonium) and the effect of these drugs on chick, mouse, cat and rat blood plasma enzyme activity was studied. Galanthamine proved to bind with acetylcholinesterase in the anionic areas of the catalytic centres, oxazyl interacted in the area of the allosteric anionic site, and tacrin interacted with the hydrophobic areas of the enzyme.

Allosteric Site↗
PubMedDate not supplied

[Comparison of anticholinesterase activity and the effectiveness of anticholinesterase substances].

In vitro tests set up to compare the anticholinesterase, cholinomimetic, cholinopotentiating and cholinolytic activity of 6 reversible cholinesterase inhibitors furnished grounds for an inference that all these agents produce an anticholinesterase effect which determines the qualitative specificity of their action. This specificity has been demonstrated in experiments on cats and rabbits. Some of the drugs (oxazyl) exert a practically elective effect on the H-cholinoreactive muscle systems, whereas others (eserin) act in a similar manner on the M-cholinoreactive systems of the intestines. The action of proserine and galanthamine os of a less selective nature.

Ambenonium Chloride↗