6533b857fe1ef96bd12b3ac3

RESEARCH PRODUCT

Pancuronium improves the neuromuscular transmission defect of human organophosphate intoxication.

Roland BesserThomas VogtLudwig Gutmann

subject

MaleInsecticidesNeuromuscular transmissionNeuromuscular JunctionAction PotentialsSuicide AttemptedElectromyographyNeurotransmissionIsoindolesOrganophosphate poisoningSynaptic TransmissionNeuromuscular junctionOrganophosphate PoisoningmedicineHumansPancuroniumAxonAcetylcholine receptormedicine.diagnostic_testParathionbusiness.industryMusclesOrganothiophosphatesOrganothiophosphorus Compoundsmedicine.diseaseAntidromicMedian Nervemedicine.anatomical_structureAnesthesiaNeurology (clinical)business

description

Two patients with acute severe organophosphate intoxication showed (1) single evoked compound muscle action potentials (CMAP) with repetitive discharges and (2) prominent decremental responses of CMAP with 20 and 50 Hz supramaximal nerve stimulation. Following the intravenous injection of single small doses of pancuronium, marked improvement in these abnormalities occurred and persisted for several hours. We postulate that the physiologic improvement following low-dose pancuronium results from blockade of acetylcholine receptors, especially those located on the terminal axon responsible for antidromic backfiring.

yearjournalcountryeditionlanguage
1990-08-01Neurology
10.1212/wnl.40.8.1275https://pubmed.ncbi.nlm.nih.gov/2166248