2. • Neuromuscular blocking agents are the drugs that
act peripherally at the neuro muscular junction to
block neuromuscular transmission.
• These agents are used in order to relax and reduce
muscle tension
• They are also used to facilitate muscle relaxation
for surgery or mechanical ventilation or in ICU.
2
3. Skeletal muscle relaxants are the drugs that act
peripherally at the neuromuscular junction or
muscle fibre itself or in cerebrospinal axis to
reduce muscle tone and cause muscle paralysis.
The drugs which act at the neuromuscular junction
are used in conjunction with general anesthetics to
provide muscle relaxation during surgery.
The centrally acting muscle relaxants are used
mainly for painful muscle spasms and spastic
neurological conditions.
3
4. Curare is a generic
term for various South
American arrow
poisons. The drug has
been used for
centuries by Indians
along the Amazon and
Orinoco rivers for
immobilizing and
paralyzing wild animals
used for food; death
results from paralysis
of skeletal muscles.
4
7. Action potential
Release of Ach at motor end plate
Binding of Ach to nicotinic receptors
Increased Na+ and K+ conductance in end plate
membrane
Generation of end plate potential
Generation of action potential in muscle fibers.
Inward spread of depolarization along T tubules.
Release of Ca+ from the sarcoplasmic reticulum
Muscle contraction.
7
8. These agents act by depolarizing the skeletal
muscle and hence are called depolarizing muscle
relaxant.
At present , only a single depolarizing agent,
succinylcholine, is in general clinical use .
It should be avoided in younger children unless
absolutely necessary, because of risk of
hyperkalaemia and cardiac arrhythmia is higher.
8
9. • Mechanism of action :
Phase I block
Succinyl choline causes opening of the channels by:
1- Reacting with the nicotinic receptors (Nm)
2- Entering the channel and increasing ionic conductance .
This causes depolarization of the motor end plate which causes
contraction.
As the succinyl choline is not metabolized at the synapse,
depolarization persists and the depolarized membranes
remain unresponsive to subsequent impulses.
Phase II (Desensitization):
With continued exposure to succinylcholine , the membrane
becomes depolarized and cannot be repolarized again
(desensitized).
9
11. Therapeutic uses:
Most commonly used to facilitate intubation.
Electroconvulsive therapy.
Side effects :
Fasciculation
Muscle pain
Hyperkalemia
Malignant hyperthermia
Apnoea
11
12. These are also called as competitive blockers.
The competitive blockers have affinity for the
nicotinic cholinergic receptors at the muscle end
plate.
It consists of drugs like D-tubocurarine which
because of its long duration of paralysis needing
pharmacological reversal, is not used now.
12
13. It causes allergic reactions.
It causes the most histamine release which can lead
to bronchospasm,hypotension, salivary secretions.
The newer drugs have fewer side effects and
superior pharmacokinetic profiles than d-
Tubocurarine.
It is the main active ingredient in the South
American arrow poison – curare.
13
14. Mechanism of action :
These drugs combine with nicotinic receptors and
prevents acetylcholine binding .
As they compete with acetylcholine for receptor
binding they are called as competitive blockers.
Thus prevent depolarization of the end plate. Hence
inhibit muscle contraction , relaxation of skeletal
muscle occurs.
Their action can be overcome by increasing conc. Of
acetylcholine in the synaptic gap
e.g. Neostigmine , physostigmine , edrophonium
14
16. Neuromuscular blocking agents are used mainly in
anesthesia to produce muscle relaxation.
They are given intravenously but differ in their rate
of onset and recovery.
Most of the non depolarizing agents are
metabolized by the liver or excreted unchanged in
the urine .
They cross blood brain barrier poorly(they are
poorly lipid soluble).
Most of the peripheral NM blockers are quaternary
compounds and hence not absorbed orally.
16
