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• W2080485191 abstract "Cocaine is among the more lethal drugs of abuse. Its classic stimulant toxicity results from modulation of excitatory amino acids, central nervous system stimulation, and blockade of the reuptake of catecholamines. When combined, these properties produce the characteristic sympathomimetic toxic syndrome that includes hypertension, tachycardia, hyperthermia and severe psychomotor agitation. Additional toxic effects include blockade of both neuronal and cardiac sodium channels and blockade of cardiac potassium channels. The ability of cocaine to modulation of cardiac channels classifies it best as a type IC antiarrhythmic agent. Importantly, since type I antiarrhythmics demonstrate use-dependent blockade (ie they are more toxic at faster heart rates) the sympathomimetic effects act synergistically to exacerbate cocaine-induced cardiotoxicity. Sudden death most likely results from either direct anesthesia of the central medullary sites that control respiration and cardiac function or malignant cardiac rhythms. While true tolerance to cocaine plays little if any role in toxicity, toxicogenetics may contribute to idiosyncratic responses to cocaine. Specifically, among the three basic metabolic pathways of cocaine, the role of plasma cholinesterase (also known as butyryl cholinesterase or pseudocholinesterase) has been extensively studied. Since plasma cholinesterase (PChE) has no known function in normal life, wide variations in PChE activity are described in clinically normal individuals. Additionally, PChE is inhibited by a variety of pharmaceuticals and toxins and greatly influenced nutritional status. Since PChE controls the only pathway that converts cocaine to a non-toxic metabolite, it's function may greatly influence individual responses to the drug. Current treatment for cocaine toxicity is largely supportive and emphasizes sedation, volume resuscitation and cooling, with the occasional use of direct acting vasodilators. New therapies are targeting cholinesterase in an attempt to enhance metabolism to nontoxic metabolites. Although this approach is scientifically interesting it is unclear as to whether it can be applied to clinical events." @default.
• W2080485191 created "2016-06-24" @default.
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• W2080485191 date "2010-07-01" @default.
• W2080485191 modified "2023-09-26" @default.
• W2080485191 title "Cocaine—why so lethal?" @default.
• W2080485191 doi "https://doi.org/10.1016/j.toxlet.2010.03.077" @default.
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