Search results for "Pancuronium"
showing 3 items of 3 documents
A quantitative study of the pancuronium antagonism at the motor endplate in human organophosphorus intoxication
1995
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 b…
Pancuronium improves the neuromuscular transmission defect of human organophosphate intoxication.
1990
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.
High pancuronium sensitivity of axonal nicotinic-acetylcholine receptors in humans during organophosphate intoxication.
1991
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 respo…