High pancuronium sensitivity of axonal nicotinic-acetylcholine receptors in humans during organophosphate intoxication.
The effect of low-dose pancuronium on neuromuscular transmission was studied in 2 patients during the early and late stages of severe organophosphate intoxication. Single evoked compound muscle action potentials (CMAP) were followed by repetitive discharges and a decrement-increment (D-I) phenomenon with 10-, 20-, and 50-Hz supramaximal nerve stimulation. Intravenous pancuronium, 1 mg, abolished the D-I phenomenon, while the repetitive discharges of the CMAP were only partially reduced. It is postulated, that the disappearance of the D-I phenomenon with persistence of the CMAP repetitive discharges results from blockade of nicotinic-acetylcholine receptors located on the terminal axon responsible for stimulus-induced antidromic backfiring. This response to a very low dose of pancuronium indicates a high sensitivity of the axonal nicotinic-acetylcholine receptor to pancuronium in humans, as had been previously postulated from animal experiments.
Besser
R
R
Department of Neurology, University of Mainz, FRG.
Vogt
T
T
Gutmann
L
L
Wessler
I
I
D005071:Evoked Potentials / Q000187:drug effects; D005260:Female; D006801:Humans; D007306:Insecticides / Q000506:poisoning*; D008297:Male; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology*; D009946:Organothiophosphorus Compounds; D010197:Pancuronium / Q000494:pharmacology*; D017981:Receptors, Neurotransmitter / Q000187:drug effects; D011978:Receptors, Nicotinic / Q000187:drug effects*; D009435:Synaptic Transmission / Q000187:drug effects
D007306:Insecticides; D009946:Organothiophosphorus Compounds; D017981:Receptors, Neurotransmitter; D011978:Receptors, Nicotinic; D010197:Pancuronium