Kinetics of intravenous pyridostigmine in man.

Calvey, T. N.; Chan, Kelvin; Dehghan, Arash; Williams, N. E.

doi:10.1111/j.1365-2125.1981.tb01146.x

Cited by 9 publications

(3 citation statements)

References 7 publications

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“…In several investigations, secondary plasma concentration peaks have appeared at variable times after oral doses of pyridostigmine (Calvey et al 1981;Chan et al 1981;Davison et al 1981 ;White et al 1981). The secondary rise has been claimed to be due to the formation of ion pairs with intestinal components such as mucin or bile salts; the ion pairs are then absorbed due to their more lipophilic properties Chan et al 1981).…”

Section: Neostigmine and Pyridostigminementioning

confidence: 92%

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Clinical Pharmacokinetics of Cholinesterase Inhibitors

Aquilonius

Hartvig

1986

Clinical Pharmacokinetics

101

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This review deals mainly with the pharmacokinetics of the reversible quaternary cholinesterase inhibitors neostigmine, pyridostigmine and edrophonium, which are mainly used to antagonise non-depolarising neuromuscular blockade in general anaesthesia and in the symptomatic treatment of myasthenia gravis. Only in the last few years, since the introduction of highly sensitive and selective analytical procedures based on gas and liquid chromatography, have proper pharmacokinetic studies of these drugs become possible. Rapid cooling and addition of internal standard to samples before freezing are important precautions in view of the poor stability of the cholinesterase inhibitors in plasma and blood. Plasma clearances of the reversible quaternary cholinesterase inhibitors are in the range 0.5 to 1.0 L/h/kg and their apparent volumes of distribution range from 0.5 to 1.7 L/kg. Accordingly, the drugs have short plasma elimination half-lives, in the order of 30 to 90 minutes. One to two hours after oral administration of 60 mg pyridostigmine, peak plasma concentrations of 40 to 60 micrograms/L are observed, whereas the plasma concentrations of neostigmine after a 30 mg oral dose are only 1 to 5 micrograms/L. The oral bioavailability of these hydrophilic ionised compounds is low: that of pyridostigmine is approximately 10% and the value for neostigmine is even lower. In spite of the short elimination half-life of pyridostigmine, intraindividual variations in plasma concentration during a dose interval are small in myasthenic patients receiving oral maintenance therapy, probably as a result of slow absorption from the gastrointestinal tract. Severely impaired renal function has been shown to prolong the elimination of neostigmine and pyridostigmine, while methylcellulose has been reported to inhibit the absorption of the latter drug completely. Other pharmacokinetic drug interactions suggested so far do not seem to be of clinical significance. Although a positive correlation has been demonstrated between the plasma concentrations of these drugs and their pharmacological effects as measured by a decrement in muscle response to repetitive nerve stimulation in a single muscle, this relationship is less clear when a global evaluation of muscular function in myasthenia gravis is used. Pharmacokinetic studies of the tertiary reversible cholinesterase inhibitor physostigmine, an important tool in experimental cholinergic neuropharmacology, are still in their initial stages. This drug too is characterised by a short plasma elimination half-life of 20 to 30 minutes.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Neostigmine and Pyridostigminementioning

confidence: 92%

“…The higher volume of distribution of pyridostigmine as compared with neostigmine is probably due to the enhanced tissue sequestration of the former drug (Calvey et al 1981). The apparent volume of distribution of neostigmine has been found not to differ between infants, children and adults (Fisher et al 1983) [see also section 3.1].…”

Section: Distributionmentioning

confidence: 98%

Clinical Pharmacokinetics of Cholinesterase Inhibitors

Aquilonius

Hartvig

1986

Clinical Pharmacokinetics

101

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“…Estimates of the distribution half-life of PB have included 0.12 (Croimelly et al 1980) and 0.14 hours (Breyer-Pfaff et al 1985). Some tissue sequestration of PB presumably occurs (Calvey et al 1981), but neither PB nor its main metabolite is bound to plasma proteins or within red blood cells (Komfeld et al 1970). Under ordinary conditions, the positively charged nitrogen of the pyridostigmine moiety of PB prevents it from crossing an intact blood-brain barrier, although this barrier may normally be at least partially permeable to polar compounds such as pyridostigmine, specifically in the fourth ventricle and in the brainstem (Dunn et al 1997).…”

Section: How Is Pb Distributed In the Body?mentioning

confidence: 99%

Clinical Considerations in the Use of Pyridostigmine Bromide as Pretreatment for Nerve-Agent Exposure

Madsen¹,

Hurst²,

MacIntosh³

et al. 2003

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