Abstract
During the past decade considerable advances have been made in the development of therapeutic antidotes against organophosphorus cholinesterase (ChE) inhibitors. Poisoning with most organophosphorus anticholinesterases (AntiChE) is treatable with a combination of an antimuscarinic compound, such as atropine sulfate (ATS), and an oxime, such as pralidoxime chloride (2-PAM) or toxogonin (18, 30, 34). The antidotal effects of oximes are generally thought to be due to their ability to reactivate the inhibited cholinesterase enzyme (10, 25, 26); however, a part of their beneficial effect has been ascribed to actions other than enzyme reactivation (4, 35, 41). Since most of the useful oximes are quaternary in structure and do not readily cross the blood brain barrier, the role played by the oximes in the central nervous system (CNS) is in some doubt (3, 25, 52). Although small quantities of these oximes do enter the central nervous system, the degree of reactivation of brain ChE is not great (11, 15).
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© 1986 Plenum Press, New York
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Shih, TM., Whalley, C.E., Valdes, J.J., Lundy, P.M., Lockwood, P.A. (1986). Cholinergic Effects of HI-6 in Soman Poisoning. In: Hanin, I. (eds) Dynamics of Cholinergic Function. Advances in Behavioral Biology, vol 30. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5194-8_75
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