6533b870fe1ef96bd12cf368
RESEARCH PRODUCT
High pancuronium sensitivity of axonal nicotinic-acetylcholine receptors in humans during organophosphate intoxication.
Thomas VogtRoland BesserIgnaz WesslerLudwig Gutmannsubject
Nervous systemMaleInsecticidesPhysiologyNeuromuscular transmissionNeuromuscular JunctionNeurotransmissionPharmacologyReceptors NicotinicSynaptic TransmissionNeuromuscular junctionCellular and Molecular NeurosciencePhysiology (medical)medicineHumansPancuroniumAxonEvoked PotentialsAcetylcholine receptorChemistryOrganothiophosphorus CompoundsAntidromicReceptors Neurotransmittermedicine.anatomical_structureNicotinic agonistAnesthesiaFemaleNeurology (clinical)description
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1991-12-01 | Musclenerve |