Clinical use
- An agent used to provide muscle relaxation and diminish reflexes
- This is useful for tracheal intubation and surgery
Mechanism of action
- Impairs cholinergic transmission at the neuromuscular junction
Agents
Nicotinic receptor antagonists (aka Non-depolarizing neuromuscular blockers)
- Medications
- Atracurium, mivacurium, pancuronium, rocuronium, tubocurarine, and vecuronium
- Mechanism of action
- Competes with acetylcholine for binding of nicotinic receptors on the motor-end plate → prevents depolarization → inhibiting muscle contraction
- Antidote
- By increasing the acetylcholine concentration in the neuromuscular junction with acetylcholinesterase inhibitors (e.g., neostigmine) overcomes the antagonistic effect of these non-depolarizing agents
- Administer with atropine to prevent off-target muscarinic effects
Nicotinic receptor agonists (aka Depolarizing neuromuscular blockers)
- Medication
- Succinylcholine
- Mechanism of action
- Binds to nicotinic receptors; however, they are more resistant to acetylcholinesterases than acetylcholine → constant stimulation of the receptor
- Phase I depolarization
- Prolonged depolarization at the receptor
- There is no antidote and block is potentiated by acetylcholinesterase inhibitors
- Paradoxical, but acetylcholinesterase inhibitors may inhibit other cholinesterases that do break down succinylcholine (e.g., pseudocholinesterase)
- Can manifest as fasciculations
- Phase II depolarization
- Repolarization, thus making the receptor unable to transmit further electrical impulses
- Antidote
- Acetylcholinesterase inhibitors
- Adverse effects
- Malignant hyperthermia
- Hyperkalemia
- Especially in burn patients or those with extensive tissue damage
- Denervating neuromuscular diseases (e.g., ALS or MS) secondary to upregulation of ACh receptors
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