PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Armin”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1981

[Effect of armin on synaptic transmission in frog neuromuscular preparations].

The action of armin, an organophosphorus inhibitor of cholinesterases, on synaptic transmission parameters was studied by means of intracellular registration of end plate potentials and currents (EPP and EPC) in the frog. On 10-minute exposure the increase in the temporary parameters became manifest provided the drug was administered at a concentration of 10(-6) g/ml and over. EPC reversal potential and cholinoreceptor sensitivity to armin did not change substantially. At a concentration of 10-(-8) g/ml armin exerted a potentiating effect on the frequency of miniature EPP and quantum composition of EPP, while that effect was not related to armin anticholinesterase activity. The presynaptic acetylcholine release was suppressed by high concentration of armin (10(-5) g/ml). Under the conditions cited there was a decrease in the depot of the available transmitter quanta in nerve terminals.

Acetylcholine↗
PubMed1979

[Effect of armin on the ultrastructure of the neuromuscular synapse].

Alterations induced by the cholinesterase inhibitor armin (5.10(-7) g/ml) in the ultrastructure of motor nerve endings of the rat phrenic diaphragmal preparations at rest or electric stimulation of the nerve were studied. It was shown that armin at rest induced ultrastructural lesions in the endings similar to those in the control preparations during nerve stimulation. Electric stimulation did not produce additional changes in the ultrastructure of the neuromuscular junction under armin action. It is suggested that the disorder of the nerve ending function may be of importance in the mechanism of the blocking action of armin on the neuromuscular transmission.

Animals↗
PubMed1983

[Effect of armin on frog myelinated nerve fibers].

Study of the action of armin on the nodes of Ranvier in isolated nerve fibers of the frog has demonstrated that armin at concentrations over 4 X 10(-7) M produces the growth of the input resistance of the nodes of Ranvier at the expense of the decreased leakage conduction. At concentrations of 4 X 10(-6) and 4 X 10(-5) armin leads to a shift of the firing level of action potentials towards more positive values.

Action Potentials↗
PubMedDate not supplied

[Effect of armin and dipyroxime on the nicotinamide coenzyme and adenine nucleotide content of the rat myocardium and liver].

It has been shown in rat experiments that armin in doses that inhibit blood cholinesterase by 50 and more per cent lowers the content of nicotinamide coenzymes in the myocardium and liver of the animals, primarily at the expense of the diminution of the oxidized forms. In the rat liver, armin decreases the content of adenyl nucleotides, mainly at the expense of ATP. Dipyroxime prevents changes induced by armin, which is accompanied by partial reactivation of cholinesterase. It is suggested that in the mechanism of antidote action of dipyroxime, of importance is its normalizing effect on redox and energy processes in the body.

Adenine Nucleotides↗
PubMedDate not supplied

[Allergenic action of armin].

The allergic effect of armine--ethyl paranitrophenyl ether of the ethylpohosphinic acid--was studied. Armine was injected subcutaneously in doses of 0.1, 0.01, 0.005 and 0.0005 mg/kg to guinea pigs 5-6 times at intervals of 2-3 days. The challenging introduction of armine in a dose equalling the sensitizing one produced an anaphylactic shock in a group of animals sensitized with single doses of 0.005 and 0.0005 mg/kg. The allergic nature of these reactions was also confirmed by a large number of positive results secondary to immunological tests preceding the challenging dose, viz. by degranulation of mast cells, agglomeration of leucocytes and passive skin anaphylaxis.

Allergens↗
PubMedDate not supplied

Acetylcholine and cholinesterase in submandibular glands of rats given armin and obidoxime.

The effects of obidoxime, a pyridinium oxime, on the cholinesterase activity and acetylcholine content of the submandibular glands of rats poisoned with armin, an organophosphorus anticholinesterase agent, were studied. The results indicate that obidoxime-induced reactivation of phosphorylated cholinesterase can suppress completely the increase in the concentration of acetylcholine that develops within the submandibular gland after administration of armin alone.

Acetylcholine↗
PubMedDate not supplied

[Nonquantal mediator secretion in the synapses of the mouse diaphragmatic preparation to the administration of sublethal doses of armin].

During in vivo experiments on the mouse diaphragm preparations the effect of a single sublethal dose of armin (1/2 of LD50) on the dynamics of changes in acetylcholinesterase activity, frequency and time of half-decay of miniature end-plate potentials (MEPP) was studied as compared with the H-effect value. It was found that the increase of the H-effect correlated (r = 0.902) with the decrease of acetylcholinesterase activity, the increase of MEPP frequency occurring later than the changes in the enzyme activity and the H-effect value. The data obtained reveal the possible of nonquantal secretion of the mediator from the motor nerve endings of the skeletal muscles in the pathogenesis of acute poisonings with armin.

Acetylcholine↗
PubMedDate not supplied

[Toxic and pharmacological characteristics of armin and nibufin homologs].

The experimental studies of alkylesters of phosphonic and phosphinic acids, close homologues of armine and nibufin, showed this series of compounds to have a strongly marked anticholinesterase action. All the substances produce an inhibitory effect on the central nervous system, raise the tone of the smooth muscles on an isolated strip of rabbit small intestine and induce a miotic pupil in the animals. Introduction of butyl radicals into molecules of phosphonic acid derivatives results in diminution of toxicity and a slight decrease in anticholinesterase activity. By their properties butyl paranitrophenyl esters of ethyl- and butylphosphonic acids are closely related to armine and nibufin.

Animals↗
PubMed1983

[Presynaptic action of armin and galantamin on mammalian neuromuscular junction].

Actions of the two cholinesterase inhibitors: armin and galanthaamine on the neuromuscular transmission and on the spontaneous and evoked acetylcholine release were studied in the rat diaphragm. High concentrations (greater than or equal to 10(-6) g/ml) of these agents exhausted the available transmitter store which decreased the quantum content of e. p. p. sin single nerve stimulation. At the repetitive stimulation (10-100 s-1), armin and galanthaamine accelerated the presynaptic depression of e. p. p. s and slowed down the rate of transmitter mobilization. This resulted in a rapid decrease of quantum content and amplitude of e. p. p. s. The found presynaptic deteriorations together with the stationary postsynaptic depolarization may cause the neuromuscular block.

Action Potentials↗
PubMedDate not supplied

[Effect of armin on the microcirculation of the cerebral cortex of white rats].

Experiments on white male Wistar rats with the use of the cinetelevision technique have shown that armine in a single LD50 provokes a 85-100% increase in the blood flow rate in the microvessels and a 45-50% elevation of the diameter of the pial arterioles. Administration of the drug in a dose of 1/2 of the LD50 brings about a 90% increase in the blood flow rate, whereas the diameter of the arterioles declines by 25%. The LD50 of armine lowers the cholinesterase activity in the brain and blood by 50-60%, while 1/2 of the drug LD50 by 20-30%.

Animals↗
PubMed1976

[Effect of the cholinesterase inhibitor armin on meuromuscular synapse function of the frog sartorius muscle].

The organophosphurus inhibitor of cholinesterases armin(2-10-9--2-10-4 M) prolonged postjunction potentials and in concentration 2-10-9--2-10-7 M increased the amplitude of miniature end-plate potentials (m. e. p. p. s and quantum content of e.p.p.s. These parameters were increased again after washing. Thus, armin (2-10-9--2-10-7 M) exerts anticholinesterase effect only. In concentrations 2-10-6--2-10-4M, in addition to the anticholinesterase effect, it affects presynaptic membrane and inhibits postsynaptic membrane cholinoreceptors.

Animals↗
PubMedDate not supplied

[Protection of mice by carbamates cholinesterase inhibitors against poisoning by armin and its dependence on certain physico-chemical indicators].

A series of aminostigmin derivatives with various substituents at nitrogen in the second position of the pyridine ring, has been tested. The efficacy of preventing the death of mice poisoned by armine in five of the seven substances correlates with the constant of the rate of carbamylation of acetylcholinesterase in the in vitro experiments and with the hydrophobic nature. It is suggested that the phenomenon of protection of animals against the toxic effect of organophosphorous compounds involves the "leaving portion" of the molecule of carbamates.

Animals↗
PubMedDate not supplied

[Changes in the lesser circulation as affected by armin].

Experiments on narcotized cats have shown that intravenous administration of armine in DL50 (0.2 mg/kg) decreases the pulmonary blood flow by 52%. The reduction of the pulmonary blood flow is accompanied by a drop of pressure in the femoral artery, development of bronchoconstriction, bradycardia and arterial hypoxemia. The pressure in the lung artery remains rather high. At the beginning of intoxication the decrease of the pulmonary blood flow correlates with bronchoconstriction in a greater degree than with other indicators and as the pathological process deepens, the reduction of the pulmonary blood flow gets closely connected with bradycardia.

Animals↗
PubMed1995

[The effect of armin on neuromuscular transmission in the frog against a background of hexadecamethonium action].

Hexadecamethonium as well as its alkylating derivatives significantly decrease the effect of organophosphorous acetylcholinesterase inhibitor armine on the amplitude and duration of the EPPs. It seems possible that these substances prevent inhibition of acetylcholinesterase. This property of the substances seems to be due to a polymethelene chain with two nitrogens as the basic part of the molecule structure.

Alkylating Agents↗