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Skeletal Muscle Relaxants

Skeletal muscle relaxants are used in various surgical procedures during anesthesia, because they decrease spasm and spasticity.

Classification

Classified into three groups

  1. Peripheral acting
  1.   Centrally acting
  2.   Locally / Directly acting

Peripherally and centrally acting drugs are also known as indirectly acting drugs.

Peripherally acting

Non Depolarizing Neuromuscular Blockers

(Act at NMJ/ Most commonly used/ Also called NM blocking agents/ antagonists)

1. Isoquinoline Derivatives

d-Tubocurarine

Atracurium

Cisatracurium

Doxacurium

Mivacurium (shortest duration of action/slow onset/increase histamine release thus cause flushing, bronchospasm)

Metocurium

Miscellaneous

Gallamine

2.  Steroid Derivatives

Panuronium (can cause moderate increase in heart rate and small increase in cardiac output but no effect on TPR, because:

  1. Vagolytic action
  2. Release of NE by nerve endings
  3. Blockage of reuptake of NE)

Pipecuronium

Rapacuronium (short acting, now withdrawn)

Procuronium (fastest acting within 60-120 seconds, hence used for tracheal intubation)

Vecuronium

Procuronium and Vecuronium are intermediate acting. Panuronium and Pipecuronium are long acting.

Depolarizing Neuromuscular Blockers (agonists)

Suxamethonium

Suxethonium

Decamethonium

Centrally acting

(Act on CNS)

Benzodiazepines

Diazepam, clonazepam, Nitrazepam

GABA Analogues

Baclofen

Progabide

Propanediol Derivatives

Mephenesin
Meprobamate

Miscellaneous Compounds

Cyclobenzaprine

Methocarbamol

Orphenadrine

Tizanidine

Directly Acting

(Act directly on muscles)

Dantrolene

Neuromuscular Junction

Motor end plate is a specialized area where there is junction of the nerve fiber with the muscle fiber. There is unusual distribution of ions in the muscle fiber:

There is more negative charge inside the membrane in the resting phase.

On arrival of the action potential, release of acetyl choline from nerve terminals occurs, which binds to post-synaptic nicotinic receptors. Stimulation of these receptors cause increased influx of Na+ ions, which leads to depolarization and contraction.

Fate of acetyl choline is that it is hydrolyzed by acetylcholine esterase.

Directly acting NM blocking agents do not interfere with the release of acetyl choline. They only interact with post-synaptic nicotinic receptors.

Botulinum Toxin A

Botulinum toxin A interferes with the release of acetyl choline. It is produced by anaerobic bacteria ‘Clostridium botulinum’. It occurs due to food poisoning and can lead to respiratory paralysis and even death of the patient. However, this is used therapeutically against bronchospasm in athletes, because of the repeated use of the limbs, there is damage to the wrist and knee joints and this toxin relaxes the muscles. It is given IM and effects start within a few days. They remain for a few months. Toxin can be repeated if required.

Continue Reading

Tubocurarine -Non Depolarizing Neuromuscular Blocker

Suxamethonium -Depolarizing Neuromuscular Blocker

Factors affecting actions of Neuromuscular blockers

Benzodiazepines as Centrally Acting Skeletal Muscle Relaxants

Baclofen and Progabide -GABA Analogues

Mephenesin and Meprobamate -Propandiol Derivatives

Cyclobenzaprine, Orphenadrine and Tizanidine

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