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Peter Mirtschin - One of the best experts on this subject based on the ideXlab platform.
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Anticholinesterases as antidotes to envenomation of rats by the death adder acanthophis antarcticus
Toxicon, 1994Co-Authors: W Flachsenberger, Peter MirtschinAbstract:The purpose of this study was to find an antidote against death adder envenomation that can be used in cases of emergency, when antivenoms are not readily available (Papua New Guinea and the Australian outback). Such an antidote should allow bite victims to survive until established treatment is possible. Death adder venom is thought to act postsynaptically at the neuromuscular junction to reduce responses to acetylcholine. This causes severe flaccid paralysis and finally death, which is usually a consequence of respiratory failure. Albino Wistar rats were injected with a lethal dose of crude death adder venom. At the onset of severe envenomation symptoms, Anticholinesterases (neostigmine and edrophonium) in conjunction with atropine sulfate were administered. At the minimum lethal dose (0.15 mg/kg) all animals survived as a result of the anticholinesterase treatment. The expected survival time of animals subjected to higher venom doses was significantly extended. These results indicate that death adder bite victims may gain valuable time, if Anticholinesterases can be administered during the initial critical stage of envenomation.
B. A. Robertson - One of the best experts on this subject based on the ideXlab platform.
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DETERMINANTS OF THE REVERSAL TIME OF COMPETITIVE NEUROMUSCULAR BLOCK BY Anticholinesterases
2016Co-Authors: G. H. Beemer, A. R. Bjorksten, P. J. Dawson, R. J. Dawson, P. J. Heenan, B. A. RobertsonAbstract:We have assessed, in 200 patients, the deter-minants of the reversal time of competitive neuromuscular block by anticholinesterase when alcuronium and atracurium neuromuscular block were antagonized by neostigmine 0.04 and 0.08 mg kg'1 and edrophonium 0.5 and 7.0 mg kg'1. A biexponential relationship was found between the reversal time (time from injection of anticholinesterase to a train-of-four ratio of 70 %) and the degree of neuromuscular block at reversal (all groups; F ratio, P < 0.05). Reversal time was determined by two processes: direct antagonism by the anticholinesterase and spontaneous recovery of the neuromuscular blocking agent, with the latter becoming the major determinant at profound levels of neuro-muscular block (0-10 % of control twitch height). Neostigmine, in the doses studied, appeared to have a higher "ceiling " of neuro-muscular block which it completely antagonized, although edrophonium had a more rapid onset of action. The reversal time for alcuronium became progressively longer relative to atracurium as neuromuscular block increased because of the slower spontaneous recovery rate. Avoidance of profound neuromuscular block at the completion of surgery is required to ensure reliable an-tagonism of the block within 5-10 min by an anticholinesterase. Neostigmine 0.08 mg kg'' was found to be the most effective agent in antagonizing profound neuromuscular block
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determinants of the reversal time of competitive neuromuscular block by Anticholinesterases
BJA: British Journal of Anaesthesia, 1991Co-Authors: G. H. Beemer, A. R. Bjorksten, P. J. Dawson, R. J. Dawson, P. J. Heenan, B. A. RobertsonAbstract:We have assessed, in 200 patients, the determinants of the reversal time of competitive neuromuscular block by anticholinesterase when alcuronium and atracurium neuromuscular block were antagonized by neostigmine 0.04 and 0.08 mg kg−1 and edrophonium 0.5 and 1.0 mg kg−1. A biexponential relationship was found between the reversal time (time from injection of anticholinesterase to a train-of-four ratio of 70%) and the degree of neuromuscular block at reversal (all groups; F ratio, P
W Flachsenberger - One of the best experts on this subject based on the ideXlab platform.
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Anticholinesterases as antidotes to envenomation of rats by the death adder acanthophis antarcticus
Toxicon, 1994Co-Authors: W Flachsenberger, Peter MirtschinAbstract:The purpose of this study was to find an antidote against death adder envenomation that can be used in cases of emergency, when antivenoms are not readily available (Papua New Guinea and the Australian outback). Such an antidote should allow bite victims to survive until established treatment is possible. Death adder venom is thought to act postsynaptically at the neuromuscular junction to reduce responses to acetylcholine. This causes severe flaccid paralysis and finally death, which is usually a consequence of respiratory failure. Albino Wistar rats were injected with a lethal dose of crude death adder venom. At the onset of severe envenomation symptoms, Anticholinesterases (neostigmine and edrophonium) in conjunction with atropine sulfate were administered. At the minimum lethal dose (0.15 mg/kg) all animals survived as a result of the anticholinesterase treatment. The expected survival time of animals subjected to higher venom doses was significantly extended. These results indicate that death adder bite victims may gain valuable time, if Anticholinesterases can be administered during the initial critical stage of envenomation.
H P Benschop - One of the best experts on this subject based on the ideXlab platform.
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new method for retrospective detection of exposure to organophosphorus Anticholinesterases application to alleged sarin victims of japanese terrorists
Toxicology and Applied Pharmacology, 1997Co-Authors: Martine Polhuijs, J P Langenberg, H P BenschopAbstract:With regard to detection of exposure to anticholinesterase, the presently used methods have the disadvantage that they cannot detect either low-level exposures with certainty or the structure of the agent and the extent of poisoning. In principle, organophosphate-inhibited butyrylcholinesterase in human plasma is the most persistent and abundant source for biomonitoring of exposure to organophosphate Anticholinesterases. Fluoride ions reactivate the inhibited enzyme readily at pH 4, converting the organophosphate moiety into the corresponding phosphofluoridate. Subsequent quantitation of the latter product provides a reliable, highly sensitive and retrospective method for detection of exposure to, or handling of, organophosphates such as nerve agents and organophosphorus pesticides. We applied the new procedure to serum samples from victims of the Tokyo subway attack by the AUM Shinriyko sect and from an earlier incident at Matsumoto. In serum of 10 of 11 victims from the Tokyo incident and of 2 of the 7 samples from the Matsumoto incident, reactivation with fluoride ions yielded sarin concentrations in the range of 0.2-4.1 ng/ml serum. Evidently, these victims had been exposed to an organophosphate with the structure PriO(CH3)P(O)X, presumably with X = F (sarin). Several applications of the new procedure to establish nerve agent and/or organophosphate (OP) pesticide exposure can be envisaged, e.g., (i) in biomonitoring of exposure for health surveillance of those handling organophosphates, (ii) in cases of alleged exposure to nerve agents and/or OP pesticides in armed conflict situations or terrorist attacks, (iii) in medical treatment of intoxication, and (iv) in forensic cases against suspected terrorists that may have handled Anticholinesterases.
Tracy K. Collier - One of the best experts on this subject based on the ideXlab platform.
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Dose-additive inhibition of chinook salmon acetylcholinesterase activity by mixtures of organophosphate and carbamate insecticides.
Environmental Toxicology and Chemistry, 2006Co-Authors: Nathaniel L. Scholz, Nathan K. Truelove, Jana S. Labenia, David H. Baldwin, Tracy K. CollierAbstract:Organophosphate and carbamate insecticides are widely detected in surface waters of the western United States. These chemicals interfere with acetylcholine-mediated synaptic transmission in the nervous systems of fish and other aquatic animals via the inhibition of AChE (acetylcholinesterase) enzyme activity. Anticholinesterase insecticides commonly co-occur in the environment. This raises the possibility of antagonistic, additive, or synergistic neurotoxicity in exposed fish, including threatened and endangered species of Pacific salmon. We extracted AChE from the olfactory nervous system of chinook salmon (Oncorhynchus tshawytscha) and investigated the inhibitory effects of organophosphates (the oxon derivatives of diazinon, chlorpyrifos, and malathion) and carbamates (carbaryl and carbofuran), alone and in two-way combinations. We found that the joint toxicity of anticholinesterase mixtures can be accurately predicted from the inhibitory potencies of individual chemicals within a mixture. This indicates that organophosphate and carbamate insecticides are noninteractive in terms of AChE inhibition and that it might be possible to estimate the cumulative neurotoxicity of mixtures by simple dose addition. Because organophosphates and carbamates are likely to have additive effects on the neurobehavior of salmon under natural exposure conditions, ecological risk assessments that focus on individual Anticholinesterases might underestimate the actual risk to salmon in watersheds in which mixtures of these chemicals occur.