Intramuscular and Intravenous Administration of Small Doses of 2-Pyridinium Aldoxime Methochloride to Man

Sidell, Frederick R.; Groff, William A.

doi:10.1002/jps.2600600823

Cited by 78 publications

(13 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The values obtained for the pharmacokinetic parameters of intramuscular 2-PAM CI in his patients were similar to those we found for an intravenous infusion of pralidoxime methylsulphate in ours. The data, however, he obtained in healthy volunteers were of the same order of magnitude as in his patients but were quite different from the data in healthy volunteers published for 2-PAM CI in the literature (Sidell and Groff 1971;Sidellet al 1972b).…”

Section: Discussioncontrasting

confidence: 59%

Plasma concentrations of pralidoxime methylsulphate in organophosphorus poisoned patients

Willems

Langenberg²,

Verstraete³

et al. 1992

Arch Toxicol

View full text Add to dashboard Cite

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. Using the same data, it was found that a concentration of 4 mg.l-1 could also be obtained by a loading dose of 4.42 mg.kg-1 followed by a maintenance dose of 2.14 mg.kg-1.h-1. In order to study the pharmacokinetic behaviour of pralidoxime in poisoned patients, this continuous infusion scheme was then applied in nine cases of organophosphorus poisoning (agents: ethyl parathion, ethyl and methyl parathion, dimethoate and bromophos), and the pralidoxime plasma levels were determined. The mean plasma levels obtained in the various patients varied between 2.12 and 9 mg.l-1. Pharmacokinetic data were calculated, giving a total body clearance of 0.57 +/- 0.27 l.kg-1.h-1 (mean +/- SD), an elimination half-life of 3.44 +/- 0.90 h, and a volume of distribution of 2.77 +/- 1.45 l.kg-1.

show abstract

Section: Discussioncontrasting

confidence: 59%

Plasma concentrations of pralidoxime methylsulphate in organophosphorus poisoned patients

Willems

Langenberg²,

Verstraete³

et al. 1992

Arch Toxicol

View full text Add to dashboard Cite

show abstract

“…This result was not unexpected as 2PAM did not reactivate AChE after BOS (Table 1). However, 2PAM has a short half-life compared to BOS, 1-1.5 h in man (Sidell & Groff, 1971), so its availability was continued by repetitive dosing. When 7 injections of 2PAM were given during the first 12 h after BOS, a smaller increase in jitter resulted measured 5 days later.…”

Section: Resultsmentioning

confidence: 99%

Protection against the effects of anticholinesterases on the latencies of action potentials in mouse skeletal muscles

Kelly¹,

Ferry²,

Bamforth³

et al. 1992

British J Pharmacology

View full text Add to dashboard Cite

1 Adult male albino mice were injected subcutaneously with an organophosphorous anticholinesterase to initiate excessive variability in the latency of indirectly elicited muscle action potentials (jitter) when assessed 5 days later. 2 Pretreatment of the mice with a single dose of pyridostigmine prevented the development of jitter after subsequent dosing with an organophosphate. 3 Treatment with one dose of pralidoxime (2PAM) prevented the development of jitter if given less than 1 h after treatment with ecothiopate, a reactivatable inhibitor of cholinesterase. Similar treatment with 2PAM after a non-reactivatable inhibitor did not prevent the development of jitter. The repeated administration of 2PAM over 12 h did ameliorate jitter. 4 Pretreatment of mice orally with a-tocopherol and N-acetylcysteine, known to prevent ecothiopateinduced myopathy, did not prevent the development of jitter after ecothiopate. 5 It is concluded that the development of jitter was a consequence of the inhibition of acetylcholinesterase, and although jitter did not develop acutely, the potential for the full development of jitter was achieved about 1 h after intoxication with ecothiopate. The development of jitter did not involve the generation of free radicals. Reduction of the early effects of intoxication with anticholinesterases by pyridostigmine or 2PAM prevented the development of jitter.

show abstract

“…Pralidoxime administered to human volunteers at a dose of 10 mg/kg by the intramuscular route produced a plasma concentration of .4 mg/L within 5 -10 min, and levels were maintained above this threshold for an hour (Sidell and Groff, 1971). Adverse effects of PAM-2 iodide in volunteers include dizziness, blurred vision, occasional diplopia, impaired accommodation, nausea, and headache (Jagger and Stagg, 1958;Sidell and Groff, 1971).…”

Section: Pralidoximementioning

confidence: 99%

“…Adverse effects of PAM-2 iodide in volunteers include dizziness, blurred vision, occasional diplopia, impaired accommodation, nausea, and headache (Jagger and Stagg, 1958;Sidell and Groff, 1971).…”

Section: Pralidoximementioning

confidence: 99%

Medical Treatment of Poisoning with Organophosphates and Carbamates

Jokanović¹

2011

Anticholinesterase Pesticides

View full text Add to dashboard Cite

Intramuscular and Intravenous Administration of Small Doses of 2-Pyridinium Aldoxime Methochloride to Man

Cited by 78 publications

References 7 publications

Plasma concentrations of pralidoxime methylsulphate in organophosphorus poisoned patients

Plasma concentrations of pralidoxime methylsulphate in organophosphorus poisoned patients

Protection against the effects of anticholinesterases on the latencies of action potentials in mouse skeletal muscles

Medical Treatment of Poisoning with Organophosphates and Carbamates

Contact Info

Product

Resources

About