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RESEARCH PRODUCT
A quantitative study of the pancuronium antagonism at the motor endplate in human organophosphorus intoxication
Roland BesserLudwig Gutmannsubject
AdultTime FactorsPhysiologymedicine.medical_treatmentNeuromuscular transmissionAction PotentialsElectromyographyMotor EndplateSynaptic TransmissionNeuromuscular junctionCellular and Molecular Neurosciencechemistry.chemical_compoundOrganophosphate PoisoningPhysiology (medical)medicineHumansPancuroniumRepetitive nerve stimulationAntidoteNeuromuscular BlockadeMovement DisordersDose-Response Relationship Drugmedicine.diagnostic_testbusiness.industryNeuromuscular DiseasesAcetylcholinesteraseElectric Stimulationmedicine.anatomical_structurechemistryAnesthesiaInjections IntravenousToxicityAcetylcholinesteraseNeurology (clinical)businessdescription
Nine patients with organophosphorus (OP) intoxication developing neuromuscular transmission defects were given pancuronium 1, 2, or 4 mg intravenously (IV). Thirteen patient controls with hypoxic encephalopathy received similar dosages. The responses were monitored electrophysiologically using single and repetitive nerve stimulation (20 and 50 Hz). In OP patients, pancuronium did not alter the amplitude of the single CMAP, whereas its repetitive discharges were reduced. Severe neuromuscular blocks were reversed only partially by pancuronium 4 mg. In less severe blocks, 1 and 2 mg resulted in marked improvement. In the patient controls, pancuronium 4 mg induced a severe neuromuscular block but not with 1 and 2 mg. Pancuronium dosages necessary to reverse severe OP-induced neuromuscular blockade produce a neuromuscular block when AChE activity is normal. Low dosages have little effect on normal neuromuscular transmission, but improve the block to a mild degree and may be useful as part of treatment in OP intoxications. 1995 John Wiley & Sons, Inc.
year | journal | country | edition | language |
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1995-09-01 | Muscle & Nerve |