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Results for “Cholinesterase Reactivators”

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At least 19 recordsLinked to original sources
PubMedDate not supplied

[The mechanism of the effect of the cholinesterase reactivator diethyxime on different models of the development of delayed hypersensitivity in acute dichloroethane poisoning].

Formation of DTH to sheep red blood cells was studied in CBA mice on different models in acute DCE poisoning (0.75 LD50). The effect of the reactivator cholinesterase diethyxime on this reaction in acute poisoning, and the relation of the reactions under study in various experimental series with the activity of alpha-naphthyl-AS-acetatesterase in the spleen cells and popliteal lymph nodes were also studied. Acute DCE poisoning (0.75 LD50) lowered cellular immunity which was assessed according to DTH formation in various models due to decrease of alpha-naphthyl-AS-acetatesterase activity in the splenocytes and cells of the of the suppressor cells in the DTH reaction. The reaction was attended with decrease of alpha-naphthyl-AS-acetatesterase in the splenocytes of the donors and the popliteal lymph nodes of the recipients apparently due to relative prevalence in the spleen cells of T-suppressors which are distinguished by poor esterase activity. Diethyxime restored completely the formation of DTH studied in different models (with the exception of the reaction in which the effect of transfer of the suppressor cells was assessed) due to restoration of alpha-naphthyl-AS-acetatesterase activity in the cells of the lymphoid organs.

Acute Disease↗
PubMed1987

Blood concentrations of 2,3-butanedione monoxime and some blood biochemical changes in Bubalus bubalis after intramuscular administration of this cholinesterase reactivator.

The blood levels of cholinesterase reactivator 2,3-butanedione monoxime were determined in buffalo calves following single intramuscular doses of 20 and 50 mg/kg body weight. Blood cholinesterases and other enzymatic activities were monitored at various times. The drug was rapidly absorbed with half-life of 0.09-0.12 h. The peak 2,3-butanedione monoxime blood concentrations of 24.7 +/- 0.3 and 38.9 +/- 1.7 micrograms/ml occurred at 10 min after 20 and 50 mg/kg doses, respectively. The elimination half-life varied between 3.05 +/- 0.12 and 3.80 +/- 0.19 h. Lack of adverse effect of 2,3-butanedione monoxime on blood cholinesterases and other enzymes indicated that intramuscular doses as high as 50 mg/kg may be safely employed in buffaloes.

Animals↗
PubMed1985

Clinical observation and comparison of the effectiveness of several oxime cholinesterase reactivators.

After passing toxicity and experimental therapeutic tests, four oxime cholinesterase reactivators [PAM (pyridine aldoxime methiodide), PAC (pralidoxime, pyridine aldoxime methylchloride), TMB4 (trimedoxime), and DMO4 (obidoxime, Toxogonin, LüH6)] were compared in clinical trials. All of them proved capable of restoring erythrocyte cholinesterase activity and relieving symptoms and signs of organophosphate insecticide poisoning. Mildly and moderately poisoned patients can be treated by several injections of any one of these drugs alone, but severe cases need the synergistic action of atropine, as well as treatments for two to three consecutive days. Although response to treatment is stronger with TMB4 and DMO4, they are not recommended for routine treatment because of their dangerous adverse side effects.

Alanine Transaminase↗
PubMed1978

The ganglionic blocking properties of the cholinesterase reactivator, HS-6.

Following intravenous administration of the cholinesterase reactivator HS-6 (30 mg/kg), blood pressure fell (up to 50 mmHg) and maximal blood levels of HS-6 reached 242 microgram/ml. HS-6 attenuated the pressor response resulting from carotid occlusion and the depressor effect of vagal stimulation. Doses of HS-6 below those used to protect against soman in different animal species (10--30 mumol/kg) progressively blocked the ganglion-stimulating effects of nicotine and dimethylphenylpiperazinium but not the pressor effect following adrenaline, a pattern similar to that produced by hexamethonium but only 1/84 as potent. HS-6, like hexamethonium and mecamylamine, progressively blocked the contraction of the nictitating membrane of the cat resulting from preganglionic stimulation. The results indicate that HS-6 possesses ganglion-blocking properties at doses likely to be used in the protection against soman poisoning. The ganglion-blocking properties of the drug may be a factor in the beneficial effects of HS-6.

Animals↗
PubMedDate not supplied

[The presynaptic mechanism of interaction of cholinesterase reactivator and muscarinic antagonists in the animal's defence in organophosphate intoxication].

The presynaptic and antidote activity of various combinations of cholinesterase reactivators and that of muscarinic antagonist were compare it was show that the mechanism of the antidote effect of some cholinesterase reactivators in poisoning with organophosphorous compounds, in addition to restoring the activity of the enzyme, includes the effect of counteraction to the effect of muscarinic antagonists in increased acetylcholine secretion into the synaptic cleft. The expression of this effect depends on the presynaptic activity of the reactivator and on the selectivity of muscarinic antagonist. It is suggested that the type relation of the presynaptic muscarin receptors in the cerebral hemispheres and the brain stem is different and that the probability of the functional value of the ligand presynaptic interaction for the protection from organophosphorous compounds is higher in the brain higher in the brain stem than in the cerebral hemispheres of rats.

Acetylcholine↗
PubMed1976

The effects of some cholinesterase reactivators on contractility of the isolated guinea-pig heart atria.

The effect of eight monoquaternary and bisquaternary pyridine aldoxime cholinesterase reactivators was tested on isolated guinea-pig heart atria. 2. Acetylcholine and methylfurthretonium in concentrations ranging from 10(-7) M to 10(-5) M have negative inotropic effects in the electrically stimulated atria and negative chronotropic effects in the spontaneously beating atria. 3. In the presence of higher concentration of cholinesterase reactivators alone, the parameters of heart muscle contractility are significantly altered. 4. Cumulative dose-response curves of methylfurthretonium in the presence of reactivators in the range of concentrations from 10(-5) M to 10(-3) M are shifted parallelly to higher concentrations of the agonist.

Acetylcholine↗
PubMed1976

Cholinesterase reactivators - contribution to the study of their metabolic effects.

Cholinesterase reactivators - trimedoxim, methoxim and obidoxim - injected in the dose of 20 mg/kg s.c., increase muscle glycogen concentration in normal, but not in adrenalectomized rats. This effect may be in connection with simoultaneously found rise of serum corticosteron level. Trimedoxim decreases adrenaline, methoxim and obidoxim noradrenaline concentration in adrenals.

Adrenal Glands↗
PubMedDate not supplied

[Central action of a new cholinesterase reactivator, diethyxime].

In anesthetized cats, whose peripheral muscarinic-cholinorecptors are blocked by m-cholinolytics (benzilyl choline) failing to penetrate into the brain, the cholinesterases reactivator diethyxime debars the centrally caused fall of the arterial pressure produced by armine, an inhibitor of cholinesterases readily gaining access into the brain. Diethyxime is also capable of abolishing the depression of the phrenic nerve action potentials produced by armine. Dipyroxime-a quaternary diethyxime analogue and also a quaternary cholinesterase reactivator fails to produce such an effect.

Action Potentials↗
PubMedDate not supplied

[Acute poisoning by insecticides with anticholinesterase activity. Evaluation of the efficacy of a cholinesterase reactivator, pralidoxime].

Pralidoxime is the most frequently used antidote in anticholinesterase insecticide poisoning, owing to its cholinesterase reactivating action. The efficiency of Pralidoxime has been retrospectively evaluated by comparing two groups of 31 patients, the first one treated by Pralidoxime in the most commonly used doses (1200mg/24H), the second one untreated. Age, sex and nature of poison were taken in consideration to make a matched distribution in both groups. The clinical and biological initial features were nearly the same in both groups; the other therapeutic measures were the same. There was no statistical difference between the both groups for evolutive criteria such as that mortality, duration of artificial ventilation, intubation, atropine administration, decrease in plasma cholinesterase. The results pleading against the use of Pralidoxime, at least at this dose, in anticholinesterase insecticide poisoning, warrant confirmation by prospective randomized studies. The efficiency of Pralidoxime warrants confirmation firstly in the course of poisonings by some clearly identified insecticides, to which pralidoxime is supposed to be the most effective, cater used in high doses, as recommended by some authors.

Cholinesterase Inhibitors↗
PubMed1991

[Cholinesterase reactivators in the combined treatment of patients with acute organophosphate insecticide poisonings].

The efficacy of different cholinesterase reactivators (alloxyme, dietixyme, dipiroxyme, isonitrosine) used as specific antidotes) was evaluated in 78 patients with acute intoxications by phosphorus-organic insecticides. The most pronounced clinical effect was obtained with use of alloxyme and dietixyme. The number of side-effects was observed during employment of dietixyme. Use of dipiroxyme with isonitrosine was less effective and was connected with a higher number of side-effects.

Acute Disease↗
PubMed1983

[Trial of cholinesterase reactivators as proserine antagonists].

HI-6 and TMB-4 were the most effective and safe of 7 cholinesterase reactivators tested as agents for the prophylaxis of proserine poisoning of male mice. The reactivator HI-6 strongly potentiated the prophylactic efficacy of a mixture of atropine and arpenal administered in the doses sufficient for the blockade of both the m- and h-cholinoreactive systems of mice. As demonstrated by experiments in vitro, HI-6 and TMB-4 did not reacivate proserine-inhibited cholinesterase. The natural anticholinesterase activity of HI-6 was negligible. Based on the correlation of the data obtained to the reported data indicating that HI-6 has a low ganglioblocking activity it is inferred that the direct effect on the receptor is of no importance for the potentiating effect. It is assumed that HI-6 modulates the cholinoreactive systems, which leads to a dramatic increase of the efficacy of cholinolytics.

Animals↗
PubMed2006

Current understanding of the application of pyridinium oximes as cholinesterase reactivators in treatment of organophosphate poisoning.

This paper reviews the mechanisms of interaction of organophosphorus compounds with cholinesterases and clinical signs of acute poisoning. Further, we describe the current understanding of the mechanisms of action of pyridinium oximes pralidoxime (PAM-2), trimedoxime (TMB-4), obidoxime (LüH-6, Toxogonin), HI-6 and HLö-7 which are used as cholinesterase reactivators in the treatment of poisoning with organophosphorus compounds. We also review the most important literature data related to the efficacy of these oximes in the treatment of poisoning with warfare nerve agents soman, sarin, tabun, VX and cyclosarin and organophosphorus insecticides. Finally, we discuss the criteria for selection of oximes intended for further development as antidotes in poisoning with organophosphorus compounds and auto-injectors for their application in urgent situations.

Animals↗
PubMed1987

Identification of two metabolites of the cholinesterase reactivator HI-6 isolated from rat urine.

Two metabolites, isolated from the urine of rats given the cholinesterase reactivator HI-6 intravenously, still contained quaternary nitrogen atoms and therefore could not be extracted from aqueous solutions by organic solvents. Both metabolites were isolated by preparative high performance liquid chromatography and were identified using mass spectrometry, gas chromatography, infrared spectrometry, ultraviolet spectrometry and proton nuclear magnetic resonance spectrometry. The structures were confirmed by in-vitro preparation of the compounds. both metabolites contained 2-pyridone moieties. One had an intact pyridinium-aldoxime moiety, and therefore could still be therapeutically active. The excretion of unchanged HI-6 together with the two identified metabolites does not provide for a 100% mass balance, indicating that in the rat, other, as yet unidentified, metabolites must be formed.

Animals↗
PubMed1996

[Comparison of the therapeutic effectiveness of selected cholinesterase reactivators with atropine in acute fosdrine poisoning in mice].

In experiments on male mice, the effect of the cholinesterase reactivators obidoxime, methoxime and HI-6 in combination with atropine sulfate on the acute intoxication with the organophosphorous insecticide fosdrine was tested in dependence on the period of administration of drugs after intoxication and on the dose of oxime by influencing the LD50 value in 48-hour survival of experimental animals. It has been demonstrated that the rate of the therapeutic intervention is a much more important factor influencing the effect of oximes than the dose of oximes. A shortening of the period of drug administration from 2 minutes to 30 seconds substantially increases the effects of all three oximes. A comparison of the effects of all three reactivators has shown that the oxime HI-6 is significantly more effective than the remaining two reactivators in the case of therapy of intoxication 30 seconds after the application of the noxa. In the therapy of intoxication 2 minutes after the exposure of experimental animals to fosdrine, the effect of the antidotal therapy was relatively low regardless of the selected oxime.

Acute Disease↗
PubMedDate not supplied

Neurobehavioral effects of the pyridinium aldoxime cholinesterase reactivator HI-6.

A series of neurobehavioral testing procedures was used to evaluate the behavioral effects of the pyridinium aldoxime cholinesterase reactivator HI-6 in male Sprague-Dawley rats. These procedures were fixed-ratio (FR) responding, shuttle-box conditioned avoidance response (CAR), conditioned taste aversion (CTA), drinking behavior, open-field exploratory behavior, negative geotaxis, and wire suspension time. Dose-response studies of HI-6 at dose-levels of 25, 50 and 100 mg/kg, or saline (IP) were evaluated. HI-6 disrupted FR responding in a dose-dependent fashion, with significant effects occurring at doses of 50 and 100 mg/kg. The pattern of disruption was characterized by extended periods of nonresponding having an abrupt onset and offset. HI-6 produced CTA in a dose-related manner, with significant effects at doses equal to those that disrupted FR performance. HI-6 did not alter CAR, drinking motivation, exploratory behavior, negative geotaxis, or wire suspension time. These data suggest that there may be a commonality in the underlying mechanism(s) for the disruption in FR performance and the induction of the CTA. This mechanism may relate to the presumed drug-induced adverse internal state inducing the CTA.

Analysis of Variance↗