The Effects of Acetyleholine, Decamethonium and Suneeinylcholine on Neuromuscular Transmission in the Rat

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<jats:title>Summary.</jats:title><jats:p>The neuromuscular block produced in the isolated nerve‐diaphragm preparation of the rat by acetylcholine, decamethonium and succinylcholine has been investigated with intracellular recording electrodes.</jats:p><jats:p>The agents investigated are found to act on the neuromuscular junction in a qualitatively similar way.</jats:p><jats:p>They cause a depolarization of the end‐plates from about 95 mV to 65–70 mV, and of regions distant from the end‐plate to about 70 mV. No significant repolarization of the muscle membrane occurs during the neuromuscular block.</jats:p><jats:p>Using high concentrations of potassium, it was found that the muscle membrane had to be depolarized to 50–55 mV in order to produce a neuromuscular block in the majority of the muscle fibres.</jats:p><jats:p>During the block of neuromuscular transmission caused by the agents investigated the muscle membrane was insensitive to the depolarizing effect of the transmitter substance.</jats:p><jats:p>It is concluded that the neuromuscular block caused by ace‐tylcholine, decamethonium and succinylcholine is not due to a depolarization of the muscle membrane, and that the block is presumably caused by a decrease in the sensitivity of the end‐plate to the transmitter substance.</jats:p>

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