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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‐l) phenomenon with 10‐, 20‐, and 50‐Hz supramaximal nerve stimulation. Intravenous pancuronium, 1 mg, abolished the D‐l phenomenon, while the repetitive discharges of the CMAP were only partially reduced. It is postulated, that the disappearance of the D‐l phenomenon with persistence of the CMAP repetitive discharges results from blockade of nicotinic‐acetyl‐choline 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.