This document discusses different classes of skeletal muscle relaxants, including neuromuscular blockers and spasmolytic drugs. It describes their mechanisms of action, pharmacokinetics, and adverse effects. Neuromuscular blockers are classified as depolarizing (like succinylcholine) or non-depolarizing (like tubocurarine and rocuronium) and work by preventing acetylcholine from acting at the neuromuscular junction. Spasmolytic drugs used for chronic muscle spasms include baclofen, diazepam, and tizanidine which act in the central nervous system, and dantrolene which acts directly on muscle.

1. Skeletal Muscle Relaxants
DR.M.USMAN KHALID
DPT,MS-NMPT

2. Classification
 Neuromuscular Blockers
 Non Depolarizing:
 Long Acting e.g Tubocurarine
 Intermediate Acting e.g.Rocuronium
 Depolarizing(Succinylcholine)

3.  Spasmolytics
 Chronic Use:
 CNS Action e.g.Baclofen,Diazepam,Tizanidine
 Muscle Action:
 E.g.Dantrolene

4. Neuromuscular Blocking Drugs
 Pharmacokinetics:
 Given Parenterally,Highly Polar(Can’t cross BBB)
 High levels it may cause seizures

5. Mechanism of Action
 Prevents action of Ach at the skeletal muscle end plate
 They compete with Ach
 Some drugs may also directly plug the ion channel operated by Ach
receptor
 Post tetanic potentiation is preserved,Tension during tetanus fades rapidly
 Larger muscles are more resistant to neuromuscular blockade

6. Depolarizing Neuromuscular Blocking
Drugs
Pharmacokinetics:
 Parenteral:
 short action
 inactivated by plasma esterases

7. Mechanism of action
 —Succinylcholine acts like a nicotinic agonist and depolarizes the
neuromuscular end plate
 When given by continuous infusion, the effect of succinylcholine changes
from continuous depolarization (phase I) to gradual repolarization with
resistance to depolarization (phase II) (ie, a curare-like block.

8. Reversal of Blockade
 Readily reversed by increasing the concentration of normal transmitter at
the receptors.
 Neostigmine or pyridostigmine

9. Adverse effects
 Respiratory paralysis
 Autonomic ganglia stimulation
 Histamine release
 Muscle pain
 Hyperkalemia
 Increased intragastric and intraocular pressure

10. Non depolarizing drugs
Mechanism of action:
 Competitive antagonists at skeletal muscle ACh-N receptor.

11. Pharmacokinetics:
 Parenteral use
 variable disposition
 Spontaneous inactivation (atracurium, cisatracurium)
 Plasma ChE (mivacurium)
 Hepatic metabolism (rocuronium, vecuronium)
 Renal elimination (doxacurium, pancuronium, tubocurarine)

12. Adverse effects
 Histamine release (mivacurium, tubocurarine)
 Laudanosine formation (atracurium)
 Muscle relaxation is potentiated by inhaled anesthetics, aminoglycosides
and possibly quinidine.

13. Spasmolytic drugs
Mechanism of action:
 Three of the drugs (baclofen, diazepam, and tizanidine) act in the spinal
cord.
 Baclofen acts as a GABAB agonist at both presynaptic and postsynaptic
receptors, causing membrane hyperpolarization.
 Presynaptically, baclofen, by reducing calcium influx, decreases the
release of the excitatory transmitter glutamic acid.
 At postsynaptic receptors, baclofen facilitates the inhibitory action of
GABA.

14. Mechanism of action:
 Diazepam facilitates GABA-mediated inhibition via its interaction with
GABAA receptors.
 Tizanidine, an imidazoline related to clonidine with significant α2 agonist
activity, reinforces presynaptic inhibition in the spinal cord.
 Dantrolene : Weakens muscle contraction by reducing myosin-actin
interaction.

15. Pharmacokinetics
 Oral
 Diazepam may also be given parenterally.

16. Adverse effects
 Sedation
 Muscle weakness
 CNS depression