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neuromuscular blocking agents block
nicotinicM receptors at the neuromuscular junction.
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The ganglionic blocking agents block
nicotinicN receptors in autonomic ganglia.
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Neuromuscular blockers interfere with
nicotinicM receptor activation and thereby cause muscle relaxation.
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Nondepolarizing neuromuscular blockers act by competing with
acetylcholine (Ach) for binding to nicotinicM receptors.
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Succinylcholine,
the only depolarizing neuromuscular blocker in use
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Succinylcholine binds to
nicotinicM receptors,
causing the end-plate to depolarize; the drug then remains bound, which keeps the end-plate from repolarizing.
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Neuromuscular blockers are used to produce
- muscle relaxation during surgery,
- endotracheal intubation,
- mechanical ventilation,
- electroshock therapy.
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Paralysis is brief because succinylcholine is
rapidly degraded by pseudocholinesterase, an enzyme present in plasma.
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Neuromuscular blockers do not reduce
consciousness or pain
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The major adverse effect of neuromuscular blockers is
respiratory depression
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Succinylcholine can cause
malignant hyperthermia, a life-threatening condition.
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