Analysis of the organophosphate-induced electromyographic response to repetitive nerve stimulation: Paradoxical response to edrophonium and D- tubocurarine

Ricardo A Maselli, B. C. Soliven

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

We studied the mechanism underlying acute organophosphate intoxication (OPI) through in-vivo and in-vitro electrophysiologic studies in rats injected with diisopropylfluorophosphate. Intoxicated rats showed weakness, repetitive compound muscle action potentials (CMAPs) in response to a single stimulus, and decremental response to repetitive nerve stimulation that was most pronounced at the second CMAP. The decrement was worsened with the administration of edrophonium, and was completely reversed by D-tubocurarine. In-vitro microelectrode studies showed no reduction in the amplitude of miniature endplate potentials (MEPPs) or in the quantal content of end-plate potentials (EPPs). However, the half-decay times of MEPPs and EPPs were significantly prolonged. Trains of stimuli induced sustained end-plate depolarization via a 'staircase phenomenon' of summation of prolonged EPPs, which was enhanced by edrophonium and abolished by D-tubocurarine. These results indicate that sustained end-plate depolarization can directly account for the decrement and weakness in acute OPI.

Original languageEnglish (US)
Pages (from-to)1182-1188
Number of pages7
JournalMuscle and Nerve
Volume14
Issue number12
StatePublished - 1991
Externally publishedYes

Fingerprint

Edrophonium
Tubocurarine
Organophosphates
Excitatory Postsynaptic Potentials
Action Potentials
Isoflurophate
Muscles
Microelectrodes
In Vitro Techniques

Keywords

  • end-plate
  • neuromuscular transmission
  • organophosphate

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

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N2 - We studied the mechanism underlying acute organophosphate intoxication (OPI) through in-vivo and in-vitro electrophysiologic studies in rats injected with diisopropylfluorophosphate. Intoxicated rats showed weakness, repetitive compound muscle action potentials (CMAPs) in response to a single stimulus, and decremental response to repetitive nerve stimulation that was most pronounced at the second CMAP. The decrement was worsened with the administration of edrophonium, and was completely reversed by D-tubocurarine. In-vitro microelectrode studies showed no reduction in the amplitude of miniature endplate potentials (MEPPs) or in the quantal content of end-plate potentials (EPPs). However, the half-decay times of MEPPs and EPPs were significantly prolonged. Trains of stimuli induced sustained end-plate depolarization via a 'staircase phenomenon' of summation of prolonged EPPs, which was enhanced by edrophonium and abolished by D-tubocurarine. These results indicate that sustained end-plate depolarization can directly account for the decrement and weakness in acute OPI.

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