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NEUROMUSCULAR JUNCTION BLOCKERS
Classification according to duration of action
› Short acting
Succinylcholine <8 min
Mivacurium 10-20 min
› Intermediate acting
Atracurium 25-35 min
Cisatracurium 25-40 min
Rocuronium 25-35 min
Vecuronium 25-35 min
Doxacurium more than 35 min
Tubocurarine more than 35 min
Pancuronium more than 35 min
Pipecuronium more than 35 min
Non Depolarizing / Competitive N.M Blockers- Tubocurarine etc.
Mechanism of Action:
Non Depolarizing / Competitive N.M Blockers i.e . Tubocurarine etc.
Competitive antagonist to Ach at Nicotinic (Nm) Receptor at MEP
N.M Transmission is interrupted leading to N.M. Blockade.
At Larger doses, some drugs also enter pore of ion channel of Nm ,
further decrease in N.M. Transmission.
Anticholinesterases (Neostingmine, Edrophonium,
Non depolarizing N.M. Blocker.
Chief alkaloid of curare Obtained from
Chondrodendron & Strychnos
Mono quaternary Ammonium Compound.
Not Abs. from GIT. Given I/V
It is redistributed. Not metabolised.
Excreted unchanged by kidney 40 % / Bile 60 %
Crosses Placenta but not harmful.
It does not cross BBB.
Mechanism of action:
O.O.A : 4 min.
D.OA: more than 35 min
No central effects
Skeletal muscle relaxation. First weakness &
Sequence of Paralysis of Skeletal Muscles:
Eye, Jaw, Facial muscles .
Muscles of Neck, Limbs , Trunk.
Recovery in reverse order.
Ganglionic blockade: Mild in high doses
Hypotension due to
Release of Histamine.Vasodilatation, decreased PR , decreased
Bronchoconstriction due to Histamine release
Ganglionic Blockade (Vasodilatation) in larger doses.
› Steroidal quaternary ammounioum compund
› 6 times more potent than Tubocurarine
› Quick onset of action
› No effect on ganglia
› Vagolytic effect
› Moderate increase in Blood Pressure
› No effect on CNS
› No effect on foetus
› No Histamine release
M.O A of Depolarizing drugs (Succinylcholine)
The Blockade occurs in 2 Phases
Phase I (depolarizing)
Phase I block: is augmented by anticholinestrase & not
Phase I (depolarizing)
1. Succinylcholine reacts with nicotinic receptors
2. Ion channels are opened → depolarization of motor end
3. Depolarization spreads to adjacent membrane
4. Result in disorgansed / generalized contraction of motor
5. Not hydrolyzed in synapse → persistent depolarization
→ flaccid paralysis
Phase II Block (Desensitizing Block)
With continued exposure—Initial end plate depolarization decreases
and membrane is re polarized but unresponsive/ desensitized to Ach.
Blockade of channel.
Development of in excitable area in muscle membrane immediately
surrounding the M.E.P which prevent the spread of impulses or
desensitization of membrane occurs .
When given post operatively there is rapid recovery from
even profound degree of Neuro muscular blockade.
It rapidly inactivate the steroidal neuro muscular blocking
drugs by forming an in active complex which is excreted in
MOA: It reduces the release of activator calcium from the
1/3 of oral dose is absorbed
t ½ is 8 hrs.
Initially 25mg / day gradually increase over 7
weeks to a maximum of 100 mg 4 times a day
For Malignant Hyperthemia
• Spasticity is increased muscle tone.
• increase in tonic stretch reflexes and flexor muscle spasm with
• Often observed in
– Cerebral palsy
– Multiple sclerosis
– ALS (Amyotrophic lateral sclerosis)
• Reduction of excessive skeletal muscle tone without reduction of muscle
MOA: It facilitates the action of GABA in CNS.
USES: Muscle Spasm
(local truma to tetanus)
DOSE: Oral dose initially 5 mg / day and
gradually increase to
maximum of 60 mg / day.
MOA: GABA B Agonist
• Increase in seizure activity in epileptic patients
• Excessive somnolence
• Respiratory depression
– Relieves muscles spasm. Most useful agent for
symptomatic treatment of spasticity
– Prevention of migraine
– Reduces craving in recovering alcoholics
MOA: Centrally acting Alpha 2 agonist
Inhibits release of excitatory amino acids in the
It re-inforces both pre-synaptic & post- synaptic
inhibition in the cord
Antiepileptic drug is a good spasmolytic agent in patient
with multiple sclerosis
Newer analogue of gabapentin usefull in muscle spasm
Gaba A and Gaba B agonist and has active metabolites
including GABA itself
– Absorption orally
– Highly protein bound
– Half life 12 hours
– Metabolism --- in liver by both cyotchrome P450-mediated hydroxylation and
– it inhibits glutamate release
– It also blocks postsynaptic NMDA- and kainite-type glutamate receptors and
inhibits voltage-dependent sodium channels
• 50 mg every 12 hours
• Hepatic injury
inhibitory neurotransmitter. When Given crosses
Newer drugs for treatment of ALS
Inhibit glutamatergic transmission in CNS
• Seditive, Hypnotic and Anti anxiety drug
• Its active metabolite is meprobamate.