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At least 397 records · Page 22Linked to original sources
PubMed1977

[Effect of amizil and arecoline on the activity of Na, K-ATP-ase and concentration of Na+ and K+ ions in rat brain].

A study was made of the activity of Na, K-ATP-ase and the Na+ and K+ content in the brain of rats with the action of arecoline and amizyl. Both arecoline and amizyl increased the Na, K-ATP-ase activity. This could be associated with the changes in the redistribution of the Na+ and K+ ions in the nerve cell. Arecoline proved to cause changes in the electrolyte distribution by the depolarization type, whereas amizyl--by the type of hyperpolarization of the nerve cell membrane.

Adenosine Triphosphatases↗
PubMed2003

A comparison of the neuroprotective efficacy of pharmacological pretreatment and antidotal treatment in soman-poisoned rats.

1. To study the influence of pharmacological pretreatment (PANPAL or pyridostigmine combined with biperiden) and antidotal treatment (the oxime HI-6 plus atropine) on soman-induced neurotoxicity, male albino rats were poisoned with a lethal dose of soman (54 (g/kg i.m.; 100% of LD50 value) and observed at 24 hours and 7 days following soman challenge. The neurotoxicity of soman was evaluated using a Functional observational battery and an automatic measurement of motor activity. 2. Pharmacological pretreatment as well as antidotal treatment were able to eliminate some of soman-induced neurotoxic effects observed at 24 hours following soman poisoning. The combination of pharmacological pretreatment (PANPAL or pyridostigmine combined with biperiden) and antidotal treatment was found to be more effective in the elimination of soman-induced neurotoxicity in rats at 24 hours following soman challenge in comparison with the administration of pharmacological pretreatment or antidotal treatment alone. To compare both pharmacological pretreatments, the combination of pyridostigmine with biperiden seems to be more efficacious to eliminate soman-induced signs of neurotoxicity than PANPAL. 3. At 7 days following soman poisoning, the combination of pharmacological pretreatment involving pyridostigmine and biperiden with antidotal treatment was only able to completely eliminate soman-induced neurotoxic signs. 4. Thus, our findings confirm that the combination of pharmacological pretreatment and antidotal treatment is able not only to protect the experimental animals from the lethal effects of soman but also to eliminate most soman-induced signs of neurotoxicity in poisoned rats. The pharmacological pretreatment containing pyridostigmine and biperiden appears to be more efficacious to eliminate soman-induced neurotoxic sings than PANPAL.

Animals↗
PubMed2004

Acute experimental tabun-induced intoxication and its therapy in rats.

Pharmacological pretreatment and antidotal treatment on tabun-induced neurotoxicity were studied in male albino rats that were poisoned with a lethal dose of tabun (280 microg/kg i.m.; 100% of LD50 value) and observed at 24 hours and 7 days following tabun challenge. The neurotoxicity of tabun was evaluated using a Functional observational battery and an automatic measurement of motor activity. Pharmacological pretreatment as well as antidotal treatment were able to reverse most of tabun-induced neurotoxic signs observed at 24 hours following tabun poisoning. However, there was not significant difference between the efficacy of profylaxis and antidotal treatment to eliminate tabun-induced neurotoxicity. The combination of profylactic pretreatment and antidotal treatment seems to be slightly more effective in the elimination of tabun-induced neurotoxicity in rats at 24 hours following tabun challenge in comparison with the administration of profylactic pretreatment or antidotal treatment alone. At 7 days following tabun poisoning, very few neurotoxic signs in tabun-poisoned rats were observed regardless of administration of pharmacological pretreatment or antidotal treatment. Thus, our findings confirm that the combination of pharmacological pretreatment and antidotal treatment is not only able to protect the experimental animals from the lethal effects of tabun but also to eliminate most of tabun-induced signs of neurotoxicity in tabun-poisoned rats.

Animals↗
PubMedDate not supplied

[Participation of Mg2+ and Ca2+ ions and the corresponding ATPases in the mechanism of the presynaptic action of amisyl and arecoline].

Amisyle and arecoline were found to be antagonistic drugs in the effect on content of Mg2+ and Ca2+ and on activity of corresponding ATPases in synaptosomes isolated from rat brain. Amisyle promoted the incorporation of 45Ca into synaptosomes but arecoline inhibited the reaction. The appear to be responsible for liberation and maintaining of neurotransmitters in presinaptic stores.

Adenosine Triphosphatases↗
PubMedDate not supplied

[The possible role of presynaptic effects in realizing the protective action of M-cholinolytics in dimethyl dichlorovinyl phosphate poisoning].

Under the conditions of the constancy of the postsynaptic effect of two M-cholinolytics atropine and amizil the relationship between the presynaptic and protective effects of the drugs in DDVF intoxication was studied. The indication of the level of the postsynaptic activity was the suppression by the cholinolytics of tremor reaction in rats induced by the action of arecoline. The presynaptic effect of the drugs was judged by the charge of the "bound" acetylcholine content in the brains of the animals. It was found that when administered in the equieffective by the choline-blocking activity doses, atropine to a greater extent reduced the content of the "bound" acetylcholine which was increased due to the action of DDVF and at the same time it possessed the less pronounced protective activity in intoxication with DDVF than amizil. It is supposed that the removal of the presynaptic suppression of acetylcholine release due to the anticholinesterase substance action deteriorates the prognosis of the course of DDVF intoxication.

Acetylcholine↗
PubMedDate not supplied

[The detection of amizil in studying different objects].

Amisyl possesses toxic effect and it may become an object of forensic chemical laboratory analysis. Reactions of staining with reagents Marki, Frede and sulphuric acid as well as with reagent Dragendorf-orange residue--were used for amisyl identification. Method of amisyl detection in sorbent thin layer and identification by maximum light absorption in 258 nm area was also suggested. Usefulness of methods developed for amisyl analysis during investigation of pharmacological substances and human urine was studied.

Benactyzine↗
PubMedDate not supplied

[A pharmacologic analysis of preparatory mechanisms of stereotyped activity in dogs].

In dogs with elaborated rhythmic and mozaic stereotypes of secretory and motor situational conditioned reflexes specific features were revealed in the action of some neurotropic drugs (amizyl, amedine, diphacil, pediphene, chlorpromazine and sodium oxybutyrate) on preparatory (latent) conditions of excitation and inhibition, appearing in the stabilized systems of reflexes. Pharmacological analysis has pointed to the predominantly cholinergic nature of preparatory and trigger mechanisms of alimentary conditioned activity. The blockade of M-cholinoreceptors (by means of amizyl and amedine) weakens or eliminates the preparatory conditions appearing in a dynamic stereotype and disturbs the trigger reactions within three to ten days. A pediphene blockade of H-cholinoreceptors intensifies the preparatory states.

Animals↗
PubMedDate not supplied

[Effect of amizil on phospholipid metabolism in different parts of the brain].

Effect of central M-cholinolytic amizyle on incorporation of 2-14C-acetate in phospholipids of big hemispheres, cortex of big hemispheres, cerebellum and stem was studied. In administration of amizyle the most distinct alterations were observed in cortex of big hemispheres and cerebellum. In cortex of big hemispheres the specific activity of inosine monophosphate and phosphatidyl choline were increased by 77% and 97%, respectively; the specific activity of phosphatidic acid was decreased by 63%. In cerebellum the specific activity of inosine monophosphate was decreased by 52.5% and of phosphatidyl serine was increased by 95%. Distinct alterations were not observed in the intensity of incorporation of labelled precursor into phospholipids of stem. In big hemispheres the specific activity of the only inosine monophosphate was decreased by 57%.

Animals↗
PubMed1990

[The participation of cholinergic structures at different levels in shaping the immediate adaptation of the pancreas to food quality in ontogeny].

The experiments on rats showed that the urgent enzymatic adaptations of the pancreas to the quality of food have not been inherent, but have been created in the ontogeny. These adaptations are usually absent during transition to the definitive feeding (23rd day of life). Adaptation for protein stimulant appears in the moment of taking away of mother (30th day of life) and becomes persistent for protein and fat stimulants by the 90th day of life (adult rats). The blockade of different levels' cholinergic structures prevents the normal development of urgent specific pancreas adaptations in all investigated ages.

Adaptation, Physiological↗
PubMedDate not supplied

[Effect of several neuroleptic, adreno-, sympatho- and cholinolytic substances on the development of experimental cerebral edema induced by nicotine].

The influence of some neuroleptic, adreno, sympatho- and cholinolytic substances on the development of experimental brain edema induced with nicotine was studied in tests conducted on rats. It was ascertained that marked antiedemic properties display drugs blocking the alpha-adrenoreceptors (phentolamine, dopegit), the neuroleptic chlorpromazine and central M-cholinolytics (benactizine). Weak action exert central H-cholinolytics (difacil trasentin) and the neuroleptic galoperidol. Sympatho- and beta-adrenolytics (guanethidine, alpha-methyltyrosine, obsidan), and also the neuroleptic triphthazine fail to prevent the development of an experimental brain edema. It is presumed that a brain edema induced with nicotine comes as a result of the catecholamines liberation and is also due to stimulation of alpha-adrenoreactive systems.

Animals↗
PubMed1978

[Participation of cholinergic mechanisms in realizing the effects of bicuculline].

Screening and electrophysiological methods were applied to the verification of the hypothesis on a possibility of participation of cholinergic structures in the realization of bicucullin effects. M- and N-cholinolytics (benactizine, atropine, aprophen, and pediphen) failed to arrest the convulsions induced in mice by bicucullin adminstration. At the same time substances inducing accumulation of gamma-aminobutyric acid (GABA) in the brain, i.e. aminooxycetic acid and depakin produced a manifest protective action in convulsions caused by bicucullin administration. In electrophysiological experiments there was also revealed an incapacity of M-cholinolytic benaltizine to arrest the bicucullin effects. Bicucullin proved to diminish depression of the test response in the restoration cycle of the primary response of the rat sensory motor cortex at the intervals of 40--125ms between the stimuli, whereas benactizine decreased the late facilitation of the test response at the intervals of 150--300ms between the stimuli. There was also noted no interaction between benactizine and bicucullin by this test. On the basis of these data a conclusion was drawn that bicucullin effects were caused by the block of postsynaptic GABA receptors, and were not connected with the cholinergic structures activity.

Animals↗
PubMed1990

[The influence of the posterior hypothalamus on the visual cortex in different states of the reticular formation].

In alert rabbits, stimulation of posterior hypothalamus induced short-latency responses in the visual cortex and affected the formation of the EPs to light. Depending on the intervals between the stimuli, either initial extinction of the EPs (1-15 msec) or subsequent selective facilitation of its positive component with simultaneous depression of negative (20-100 msec) one, or complete recovery of the response (200-300 msec), were observed. Aminazine and benactizine made the effect of the posterior hypothalamic stimulation on visual EPs to light less obvious and changed its dynamics. Other findings suggested an inhibitory effect of the mesencephalic RF on the activity of hypothalamo-cortical input. A role of phasic mechanism of hypothalamic control in realization of visual cortex's perceptive function, is discussed.

Animals↗