Disease relevance of (2E)-1-methyl-2-(nitrosomethylidene)pyridine

• They are instructed to self-administer atropine and pralidoxime at the first sign of nerve agent toxicity [1].
• When given intracerebroventricularly into conscious rats before soman administration (0.9 LD(50), subcutaneously), the aldoximes, like atropine but not pralidoxime, protected against respiratory depression (3,4) and bradycardia (2) [2].
• 1. Possible interactions of contrathion (pralidoxime sulfomethylate), a reactivator of phosphorylated acetylcholinesterase (AChE), with the regulation of cholinergic transmission were investigated on an identified synapse in the buccal ganglion of Aplysia californica [3].
• The clinical and toxicological data of the poisonings are discussed, as well as the potential therapeutic use of pralidoxime in organophosphate intoxication [4].
• After about 3 h the patient developed symptoms and signs of early organophosphate poisoning which were treated with atropine and pralidoxime [5].

Psychiatry related information on (2E)-1-methyl-2-(nitrosomethylidene)pyridine

• Gacyclidine was injected (i.v.) in combination with atropine/diazepam/pralidoxime at man-equivalent doses after a 45- or 30-min latency period to intoxicated primates (2 LD50) [6].
• The neurobehavioral effects of pralidoxime mesylate (P2S) were characterized in the rat by comparing standard measures such as conditioned taste aversion, operant behavior and spontaneous locomotor activity [7].

High impact information on (2E)-1-methyl-2-(nitrosomethylidene)pyridine

• Effect of intravenous thiamine on pralidoxime kinetics [8].
• The kinetics of inhibition, reactivation and aging were investigated with human erythrocyte AChE, various structurally different OP (organophosphates, -phosphonates and phosphoramidates) and oximes (obidoxime, pralidoxime, HI 6, HLö 7) [9].
• STUDY OBJECTIVE: We sought to determine the feasibility of discharging Mark 1 atropine and pralidoxime autoinjectors into small, sterile vials to facilitate the potential intramuscular injection of these antidotes, particularly pralidoxime, on a milligram per kilogram basis to small children [10].
• The second part is to compare atropine and CEB-1957 (in combination with pralidoxime) for their ability to protect against the lethality induced by 2 x LD50 of the acetylcholinesterase inhibitor sarin [11].
• Receptor-mediated presynaptic facilitation of quantal release of acetylcholine induced by pralidoxime in Aplysia [3].

Chemical compound and disease context of (2E)-1-methyl-2-(nitrosomethylidene)pyridine

• On the other hand, pralidoxime and especially obidoxime seem sufficiently effective to treat poisonings with organophosphorus insecticides that have relatively less toxicity than nerve agents [12].
• Conversely, 91% of the 23-fold variation in the ability of the oximes pralidoxime and obidoxime to protect against the toxicity of OP compounds in guinea pigs was explained by the variation in the in vitro ability of oximes to reactivate OP-inhibited AChE [13].
• Although carbamates and organophosphates may cause clinically indistinguishable physical signs, pralidoxime therapy may be contraindicated for carbamate intoxications [14].
• Consequently, pralidoxime (2-PAM) in conjunction with atropine was necessary to reverse acetylcholinesterase (AChE) inhibition and cholinergic toxicity in hens given high enough doses of chlorpyrifos to cause neuropathy [15].
• Improvement of motor function in multiple sclerosis by use of protopam chloride [16].

Biological context of (2E)-1-methyl-2-(nitrosomethylidene)pyridine

• Pralidoxime mesylate absorption and heart rate response to atropine sulphate following intramuscular administration of solution mixtures [17].
• The purpose of this study was to examine the role of acetylcholinesterase on mucociliary transport by use of a potent anticholinesterase agent, soman, and potential antagonists, atropine (muscarinic antagonist) and pralidoxime (acetylcholinesterase reactivator) [18].
• The pharmacokinetics of continuous infusion pralidoxime in children with organophosphate poisoning [19].
• Effect of some cationic drugs on the intestinal absorption of pralidoxime iodide [20].
• Hydrolysis of an acetylthiocholine by pralidoxime iodide (2-PAM) [21].

Anatomical context of (2E)-1-methyl-2-(nitrosomethylidene)pyridine

• Concentrations of 2-hydroxyiminomethyl-N-methylpyridinium ion in plasma and aqueous humor as indices of the toxicity of pralidoxime mesylate (P2S) for the rabbit [22].
• The fiber necrosis of the diaphragm muscle was quantified by a morphometric technique, comparing the area fraction occupied by necrotic muscle fibers in animals that received pralidoxime at different times after intoxication, i.e., 0, 1, 3, 6, and 12 h [23].
• The in vivo rat brain microdialysis technique with HPLC/UV was used to determine the blood-brain barrier (BBB) penetration of pralidoxime iodide (2-PAM), which is a component of the current nerve agent antidote therapy [24].
• Thus, mucosal hypertonicity apparently enhances net mucosal-to-serosal transfer of PAM by blocking its active secretion from serosa to mucosa [25].
• Effects of pralidoxime applied locally into the midbrain reticular formation on the hippocampal theta rhythm induced by acetylcholinesterase inhibition [26].

Associations of (2E)-1-methyl-2-(nitrosomethylidene)pyridine with other chemical compounds

• Autoinjectors containing 300 mg/mL of pralidoxime chloride in water were stored at room temperature for 8-10 years, followed by analysis for hydrogen cyanide using an ion-selective electrode [27].
• The most rapid increase in red blood cell acetylcholinesterase activity was noted within 24 h after the first treatment with oximes Pralidoxime and/or HI-6 [28].
• EEG analysis within the classical frequency bands (beta, theta, alpha, delta) demonstrated that central activity was totally restored to normal after GK-11 treatment, but remained profoundly altered in animals receiving atropine/pralidoxime/diazepam alone [29].
• Using pharmacokinetic data from healthy human volunteers in a bicompartmental pharmacokinetic model, a repeated dose scheme for pralidoxime methylsulphate (Contrathion) was developed producing plasma levels remaining above the assumed "therapeutic concentration" of 4 mg.l-1 [30].
• The effectiveness of trimedoxime, obidoxime, pralidoxime and HI-6, given with atropine and diazepam, was tested in the treatment of poisoning with 2 LD50 of the insecticides [31].

Gene context of (2E)-1-methyl-2-(nitrosomethylidene)pyridine

• The rank order in which ligands stabilized AChE was: edrophonium greater than decamethonium greater than pralidoxime chloride much greater than procainamide [32].
• The temporal profile of butyrylcholinesterase (BuChE) and in vitro pralidoxime-reactivated BuChE was studied in a cohort of 25 organophosphate-poisoned patients to examine their relationship to the development of intermediate syndrome and to understand reasons for lack of efficacy of oxime treatment [33].
• Efficacy of an adenosine A1 receptor agonist compared with atropine and pralidoxime in a rat model of organophosphate poisoning [34].
• That LIF might act as an esterase and a protease was further strengthened by the ability of pralidoxime methansulfonate (2-PAM) to reestablish LIF activity of supernatants previously inactivated by PMSF [35].

Analytical, diagnostic and therapeutic context of (2E)-1-methyl-2-(nitrosomethylidene)pyridine

• Analysis of formulations containing pralidoxime mesylate by liquid chromatography [36].
• The HPLC analysis of the solutions after being stored an additional 3-4 years at approximately 5 degrees C demonstrated that greater than 90% of the total of all measured components consisted of pralidoxime chloride [27].
• High-performance liquid chromatographic determination of pralidoxime chloride and its major decomposition products in injectable solutions [37].
• RESULTS: We found two randomized controlled trials (RCTs) involving 182 patients treated with pralidoxime [38].
• She was treated with gastric lavage, atropine and pralidoxime (PAM) [39].

References