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C.C. Chang

Publications and source records attributed to C.C. Chang.

3 recordsLinked to original sources
PubMed1994

Inhibition of the Sodium Channel by SK&F 96365, an Inhibitor of the Receptor-Operated Calcium Channel, in Mouse Diaphragm.

The effects of SK&F 96365, a blocker of the receptor-operated Ca(2+) channel, on contractilities and the Na(+) channel of mouse diaphragm were studied. SK&F 96365 (10-50 &mgr;M) reversibly inhibited twitches, tetanic contractions and muscle and nerve action potentials. The IC(50) was 17-24 &mgr;M. The inward Na(+) current was suppressed and its recovery from inactivations delayed. Crotamine, a peptide toxin that binds to neurotoxin receptor site 3 of the muscle Na(+) channel, enhanced the inhibitory effects of SK&F 96365 and reduced the IC(50) to about 4 &mgr;M. Veratridine had similar effects, although it was less effective than crotamine. On the other hand, the crotamine-induced membrane depolarizations and spontaneous discharges of muscle action potentials were inhibited by SK&F 96365 noncompetitively. The inhibitory effects of tetrodotoxin and tetracaine were additive with those of SK&F 96365 but were enhanced slightly by crotamine. The results suggested that SK&F 96365 acts on a distinct site and blocks the Na(+) channel fo excitable membranes at a concentration range that inhibits the receptor-operated calcium channel. Copyright 1994 S. Karger AG, Basel

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PubMed1994

Editorial.

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Journal Article↗
PubMed1994

Obidoxime Antagonizes the Neuromuscular Failure Induced by Neostigmine and Diisopropyl Fluorophosphate via Different Mechanisms.

The efficacies and mechanisms of obidoxime in antagonizing the neuromuscular failure induced by neostigmine and diisopropyl fluorophosphate (DFP) were studied in mouse phrenic nerve/diaphragm preparations. Obidoxime antagonized neostigmine-induced tetanic fade (EC(50): 300 &mgr;M) by inhibiting the regenerative and sustained depolarization during repetitive stimulation. The antagonism was associated with a depression and shortening of single endplate potentials (EPPs) and miniature EPPs (MEPPs). In contrast, the neuromuscular failure induced irreversibly after treatment with DFP and followed by washout was restored by obidoxime at concentrations (EC(50): 0.6 &mgr;M) 500-fold lower than that against neostigmine. The regenerative depolarization was abolished with no depression of single EPPs and MEPPs, and the antagonistic action persisted after washout of obidoxime. The EC(50) of obidoxime was proportionately increased in the presence of increasing concentrations of DFP. Nevertheless, the EC(50) against DFP, at a concentration (30 &mgr;M) 15-fold in excess of that which caused tetanic fade, was still 10-fold lower than that which antagonized neostigmine. In both cases, the amplitudes of train EPPs were increased. It is concluded that obidoxime antagonizes neostigmine-induced neuromuscular failure by a curare-like action but antagonizes DFP by an enzyme reactivation. Copyright 1994 S. Karger AG, Basel

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