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1 Department of Anesthesiology and the Anesthesia Research Center, University of Washington School of Medicine, Seattle, Washington
Experiments were performed on rat phrenic nerve-diaphragm preparations maintained at 32 ± 2°C. Simultaneous recordings of tension output and intracellular events were made in isometrically contracting muscles. Procaine, pentobarbital and halothane depressed pro- and postjunctional structures; however, neuromuscular block under procaine and pentobarbital was of prejunctional origin whereas under halothane it could be explained by depression of postjunctional structures. Procaine and pentobarbital greatly lengthened the duration of the absolute refractory period of motor nerve terminals; this prolongation was minimal with halothane. Pentobarbjtal depolarized the end-plate membrane more than 10 mV, an effect not seen with procaine or halothane. Procaine, unlike pentobarbital or halothane affected the propagation of end-plate potentials to the muscular fiber. During tetanic stimulation of the phrenic nerve, failure to maintain strength of muscular contraction was of prejunctional origin under all three anesthetic agents; however, in most experiments under halothane the strength of these contractions increased rather than faded.
Submitted on November 2, 1970
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