Local Anaesthesia

Anaesthesia
 local anaesthesia:

Loss of sensation in circumscribed area of the body, caused

by depression of excitation or inhibition of the conduction
process in peripheral nerves, without loss of
consciousness.
 General anaesthesia:

Is the loss of all forms of sensations with loss of motor

reflexes and loss of consciousness
In dentistry, Only loss of pain sensation is desirable.
( Analgesia )
 Analagesia:

It is loss of pain sensation without loss of other

sensations and without loss of consciousness

Analgesia is a part of anaesthesia

 Local anaesthetic agents
Are drugs that block nerve conduction when
applied locally to nerve tissues in appropriate
concentrations.

Local anaesthetics acts on all types of nerve

fibres, sensory or motor. It affects the axonal
membranes of peripheral nerves.
 General anesthetics act on the synapses of the
central nervous system.
Many Methods to produce LA, some:

Reducing temperature.
Ethyl chloride spray, Is used only to produce surface
anaesthesia.

Physical
damage to nerve trunk, Nerve sectioning. Unsafe for
therapeutic uses. only in Trigeminal Neuralgia.

Chemical
damage to nerve trunk; neurolytic agents. Silver nitrate,
Phenol.
Unsafe for therapeutic use.
Anoxia or hypoxia resulting in lack of oxygen to nerve.
Unsafe as well.

Stimulation of large nerve fibres, blocking the perception of

smaller diameter fibres. Acupuncture ,TENS
(Transcutaneous Electronic Nerve Stimulation)

Drugs that block transmission at sensory nerve endings

or along nerve fibres.
The action is fully reversible and without permanent
damage to the tissues.
 Anatomy
Dendrite
Neuron is structural unit of NS.
Cell body
nucleus
Body
Dendrites

axon
Synapse
Axons (actual nerve fibers):
peripheral nervous system: may be covered by myelin
sheath (schwann cell) which allows for regrowth.
Nodes of Ranvier:
breaks in myelin.
myelin acts as resistance and insulation and
thus needs nodes for function.
Action potentials jump from node to node
 Nerve Types
motor nerves, Efferent (descending tracts)
sensory nerves , Afferent (ascending tracts)
 Pain

Definition:

Pain is incapable of definition, but it can be

defined as distressing or unpleasant sensation,
it is unique motivation which occur by noxious
stimuli (physical, chemical or thermal) through
nociceptors (pain receptors).
 Pain Threshold
amount of stimulation required before feeling
pain.

Factors that affect pain threshold:

psychological make up
fear and apprehension
fatigue
age (children and elderly have low pain threshold
than adults).
 Pain Perception
point at which a person first becomes aware of pain

Pain Reaction
physiologic and behavioral response to pain
Pain is a complex process occur in the nervous system.

Simply it is an interpretation of impulses the are

generated in the peripheral nerve endings at the site
of stimuli ( neural cell membranes) and conducted to
the brain to be translated into that unpleasant
sensation.
 Nerve conduction-depend on (ion fluxes)
across the nerve cell membrane.

Influx -entrance inside the cell

Efflux-exist from the cell

This process action potential

 Action potential

It is the change in electrical potentials that occur

between the inside and outside the nerve fiber when
it is stimulated , serving to transmit nerve signals.
The nerve cell membrane is lipid bi-layer and it
contain protein gate and Na+ k+ Pump; control
the fluxes of ions

Na+ Is the main extracellular ion

k+ Is the main intracellular ion

 Resting potential:

During rest- gate channel is closed inhibiting Na+

entry

Resulting in difference in the electrical potential

(electrical gradient) which inside (-70,-90
mV)negative to out side the concentration of Na+ is
kept as minimum by active extrusion process of Na-K
pump(as 3 Na+ out side 2 k+ inside)
Depolarization :
with the arrival of nerve impulses the gate open and
transient increase in the membrane permeability to Na+
(Na+ influx (go inside)due to concentration gradient and
it diffuse rapidly into the cell it stop by closure of the gate
which cannot reopen until repolarization

(this period of closure of the gate called refractory

period)
Firing threshold:
is the magnitude of the decrease in negative
transmembrane potential that is required to
initiate an action potential (impulse)
Repolarization:
temporary reversal of electrical polarity
resulting in out flow of k+ ion down
concentration gradient

the k+ go out side the cell (k+ efflux).

Resting potential:
the Na+ pump then extrude excess Na+ ions

accompanied by re-entry of K+ resulting in

recovery of membrane potential to it is resting
value
 The important step in nerve cell activity is
influx of Na+ ion during the firing stage

LA inhibit sodium influx.

local anesthetics:
prevents the generation and conduction of a
nerve's impulse(inhibit sodium influx) by blockade
of the Na channel.

Altering the basic resting potential of the nerve

membrane

Failure to achieve the threshold potential level

along with, depression of the rate of electrical
depolarization
 The rate of depolarization is reduced and the nerve
doesn't ever reach the firing potential.

Prolonging the rate of repolarization

Mechanism of Action of Local Anaesthesia
The following sequence is a proposed mechanism of action of local
anesthetics

1. Displacement of calcium ions from the sodium channel

receptor site, which permits ͙
2. Binding of the local anesthetic molecule to this receptor site,
which produces ͙
3. Blockade of the sodium channel, and a ͙
4. Decrease in sodium conductance, which leads to
5. Depression of the rate of electrical depolarization, and ͙
6. Failure to achieve the threshold potential level, along with ͙
7. Lack of development of propagated action potentials, which
is called ͙
8. Conduction blockade.
 Dissociation of L.A

L.A are used as salt (hydrochloride) dissolved in water or saline

it exists simultaneously as uncharged molecule (RN) also called
the base, and positively charged molecule called (RNH+), called
the cations

(RNH+) ↔ (RN) +(H+)

The relative proportion of each ionic form varies with pH of the
solution and its surrounding tissue

Also depends on pKa (dissociation constant)

 As H+ concentration increase (Low pH) the equilibrium shift to
the left, and most LA solutions exist in cationic form

(RNH+) ‹ (RN) + (H+)

As H+ concentration decrease (higher pH) the equilibrium shift

towards the free base form

(RNH+) › (RN) + (H+)

Only RN diffuse through the nerve sheath

The rate of onset of LA is related to dissociation constant (pka) of

the LA solution, it is a measure of a molecule affinity to H+
 Increasing the pH of LA solution produce more RN
form

Infection reduce the pH, so less RN form

Using Higher concentration of LA e.g. 5% lidocaine
increase the clinical efficiency (concentration
gradient)
 inflammation tends to produce lower pH in tissues
therefore:

LA are more ionized

don’t penetrate very well
decreased ability of LA to produce effects
 Tachyphylaxis

Is defined as increase tolerance to drug that is

administered repeatedly.
 Theories are:

o Calcium displacement theory.

The specific receptor binding theory.
o The membrane expansion theory.
Pharmacological actions:

o Reversible block of nerve conduction.

o Direct relaxation of smooth muscles & inhibition of neuro-

muscular transmission in skeletal muscle producing
vasodilatation.
• Intra-arterial procaine reverse arteriospasm during I.V. Sedation

o Antidysrhythmic-like action on the heart.

o Stimulation and/or depression of the CNS.

Properties of Ideal local Anaesthetic:

Possess a specific & a reversible action.

should be transient
Potency: sufficient to give complete anaesthia
without the need to use a harmful concentration
Non-irritant with no permanent damage to
tissues.
No Systemic toxicity
Active Topically or by injection
 High therapeutic ratio
Rapid onset
Suitable duration of action
Chemically stable and readily undergo
biotransformation in the body
Sterile
Be able to be administered with other agents
without loss of properties
Non allergenic
Non addictive
Chemistry:
o They are weak bases, insoluble in water

o They are composed of three parts:

Aromatic (lipophilic) .

Intermediate aliphatic chain, which is either ester or

amide link .

Terminal amino (hydrophilic) group .

LAs are Weak Bases
Intermediate chain
Aromatic portion O Amine portion
R

C O R N
R
ESTER

O R

C R N
NH
R
AMIDE

LIPOPHILIC HYDROPHILIC
 Classification

Classified according to their chemical structures and the

determining factor is the intermediate chain, into two groups:

Ester Amide

They differ in two important aspects:

Their ability to induce hypersensitivity reaction.

Their pharmacokinetics - fate and metabolism.

 Amides Esters
Longer acting Short acting
Metabolized by liver Metabolized in the plasma
enzymes and tissue fluids
(pseudocholinesterase)
Excreted in urine Excreted in urine

Articaine Cocaine
bupivacaine (Marcaine) Procaine
lidocaine ( Xylocaine)
Benzocaine
Prilocaine
lidocaine-prilocaine (EMLA) Chloroprocaine
Dyclonine
tetracaine
 Physiochemical properties

These are very important for local anaesthetic activity.

Ionization
Partition coefficiency
Protein binding
Vasodilatory effect
Ionization
They are weak base once injected in the tissue, LA exist in
both ionized and non-ionized form (this is called PK of LA)
(PK is the PH of LA solution where the ionized and non -ionized ions are in
equal distribution i.e. 50 %ionized 50% non -ionized )

The proportion depends on:

o the pKa or dissociation constant
o The pH of the surrounding medium.

Both ionizing and unionizing are important in

producing local anaesthesia.
 The lower the pKa , the more the unionized form,
the greater the lipid solubility.

The higher the pKa , the more the ionized form and
the slower the lipid solubility
 Unionized form is able to cross the bi-lipid nerve
membrane.

The ionized form then blocks conduction.

Some of the unionized inside the cell will become

ionized depending upon the pKa and the intracellular
pH (lower than extracellular)
 In general the amide type have lower pKa, and greater
proportion of the drug is present in the lipid-soluble
(unionized) form at the physiological pH

PK determine the onset of LA

( The lower the pKa the faster the onset.)
The closer the PK to the PH 7.4 of the solution the rapid
onset
E.g
Lidocaine Pk7.7 fast onset 1 - 2 minutes
Procaine 2 - 5 minutes.
 When we inject LA and exist in unionized (base) and
ionized form, the unionized form can pass through
the cell membrane (lipid bilayer) because the
unionized form is lipophilic .

This is called Partition coefficient

partition coefficient Measures the relative solubility

of an agent in fat or water
 High numerical value means:
High lipid-soluble
less water-soluble.

More fat solubility, means rapid crossing of the lipid barrier of

the nerve sheath.

The greater partition coefficient, The faster the onset

Protein binding

The duration of action is related to the degree of

binding.

Local anaesthetic agents bind with:

α1-acid glycoprotein, which possess high affinity but
low capacity.
Albumin, with low affinity but high capacity
The binding is simple& reversible
o Lignocaine is 64% bound,
o Bupivacaine is 96%
o Lignocaine 15 - 45 minutes o
Bupivacaine 6 hours
Vasodilatory ability
Most Local anaesthetics possess a vasodilatory action on blood
vessels.

It influence the duration of action of the agent.

Prilocaine is 50% bound to proteins but has a longer duration

than Lignocaine (64%) since it possess no strong vasodilatory
effect.

Affect the duration of action of the agent

 Summary

Local anesthesia temporarily blocks the normal

generation and conduction action of the nerve
impulses.

Local anesthesia is obtained by injecting the

anesthetic agent near the nerve in the area intended
for dental treatment.

Induction time is the length of time from the

injection of the anesthetic solution to complete and
effective conduction blockage.
Duration:
Length of time from induction until the reversal
process is complete.
Short-acting:
Local anesthetic agent lasts less than 30 minutes.
Intermediate-acting:
Local anesthetic agent lasts about 60 minutes.
Long-acting:
Local anesthetic agent lasts longer than 90 minutes
PHARMACOKINETICS

Uptake
Distribution
Biotransformation
Excretion
Absorption:

Many factors influence entry of local anaesthetic into

the circulation:

o Vasodilating ability of the drug.

o Volume and concentration.
o Vascularity of the tissues.
o The route of administration.
o The presence of vasoconstrictor.
Distribution:
In the circulation:

Partially bound to plasma proteins (α1-glycoprotein and

albumin) and red blood cells.
The unbound is free to enter any organ and diffuse through the
blood-brain barrier and the placenta.

Highly perfused organs such as brain, liver, kidney,

receive high level of local anaesthetic drug.
Metabolism:
This is governed by its chemical classification:

Ester Drugs:
metabolized in plasma by pseudocholinesterase
enzyme, and some in the liver.
People, who lack the enzyme, are at risk of an
overdose by the ester type local anaesthetic
Para-aminobenzoic acid (PABA) is the major
metabolite of ester with no anaesthetic effect.

It is the agent responsible for ester allergies.

Amide Drugs:
metabolized in the liver, except Prilocaine which
undergo some biotransformation in the kidney and
lungs.
Some of the metabolites possess local anaesthetic and
sedative properties.

o Normal local anaesthetic dose in patient with impaired

liver function will result in relative overdosage.
o Old age patient shows reduction in liver function

Reduce dose
Ester Group
 cocaine
The first and most potent local anaesthetic agent
Rarely used these days due to the problems of
misuse &addictive properties
Unique among local anesthetic agents in that it
produces vasoconstriction
Topical preparation as a 4 - 10% solution
Occasionally used topically intranasally during
apical surgery on maxillary incisor teeth when the
nasal floor is in close proximity.
 Procaine

The only indication for its use in dentistry, is in

patients with proven allergy to the amide group.

Used intra-arterially, as part of the recognized

regimen, to treat the arteriospasm which might
occur during intravenous sedation.

It has an excellent vasodilatory properties.

Not available as a topical agent.

Onset & duration of Action:
Has a very short duration (5 minutes) and a long
onset time of 10 minutes

Dosages:
The maximum dose is 6 mg/kg, 400 mg max.
Used as 2% with 1:80 000 epinephrine to
increase efficacy.

Metabolism:
Rapidly by plasma esterase.
Benzocaine

Most commonly used ester local anesthetic

Used mainly as topical, due to its poor water

solubility, and because of its low toxicity, it is
used in concentration up to 20%.

Hydrolyzed rapidly by plasma esterase to

P-aminobenzoic acid accounting for its low
toxicity.
Recommended uses in Dentistry:
Topical application prior to an infiltration.

Incorporated into proprietary medications for

application to painful intraoral lesions - ulcers

Sole source of anesthesia for superficial soft

tissue manipulation
Amide Group
 Lignocaine (Lidocaine)

Synthesized in 1943 and used in dentistry since

1948 and it is also known as Xylocaine

Is highly lipophilic (partition coefficient 3) ,

rapidly absorbed.

Metabolized only in the liver and its metabolites

are less toxic with no action.

Has half-life (t0.5) of 90 minutes

 Dosage:
4.4 mg/kg - 300 mg max
Used as 2% plain or with 1:80 000 epinephrine
4 and 10% spray, 2% gel and 5% ointments.

Onset & duration of action:

Rapid onset 2 - 3 minutes

With epinephrine- intermediate duration (45 - 60

minutes)
Plain- short duration (10 minutes)
Recommended uses in Dentistry:

2% with 1:80,000 adrenaline--ideal for infiltration,

intraosseous, intraligamentary, and regional block
anesthesia for majority of patients

Contraindicated
in those allergic to amides
in individuals where increased adrenaline levels
may be hazardous
Recommended uses in Dentistry:

Plain solution is not very effective in obtaining

pulpal anesthesia

Use for soft tissue procedures is very limited—

poor hemorrhage control

Nevertheless, effective topical anesthetic for non-

keratinized tissue & as a symptomatic treatment
for painful mucosal lesions such as ulcers
 Prilocaine

A very potent local anaesthetic, and is less toxic

than Lignocaine.
It produces less vasodilatation than lignocaine
Less vasoconstrictor is needed to be added.

Rate of clearance is higher than other amide-

types, suggesting extra-hepatic metabolism with
relatively low blood concentration.
 Used either plain 4% or 3% or combined with
0.03 IU/mL of Felypressin as vasoconstrictor.
Onset & Duration:
Slower onset - 4 minutes.
It’s duration of action is similar to Lignocaine.
Dosage;
6.0 mg/kg - max. 400 mg.
Combined with Lignocaine as a topical
anaesthetic agent to be used prior to
venipuncture and during dental sedation in
children.
Contraindications
Should not be administered to infants, patients with
methaemoglobineamia, kidney disease, hypoxia,
anemia, liver disease or heart failure, or any other
condition in which problems with oxygenation could
be critical; such as pregnancy.
 Mepivacaine

Possess the least Vasodilating effect.

Metabolized in the liver and has t0.5 of 120
minutes.
It’s main indication is when local anaesthetic
without vasoconstrictor is needed.
3% plain is more effective than lignocaine.

Onset & duration:

Rapid onset but slightly shorter duration.
 Bupivacaine

A long-acting local anaesthetic agent, with a t0.5 of

160 minutes due to greater binding capacity to
plasma proteins and tissue proteins

Used mainly in Oral surgical procedures for its long-

lasting pain control.
Longer onset and longer duration (Regional 6 - 8
hors)

Dosage:
1.3 mg/kg - Max 90 mg
0.25 - 0.75% with or without adrenaline 1:200
000
 Lignocaine is the most common used agent both

topically and by injection as 2% with or without

adrenaline, with a maximum dose of (300mg)

 Combination product
EMLA

EMLA = eutectic mixture of local anesthetics

Eutectic = two solid substances mixed together in
equal quantities by weight .
the melting point of the mixture is lower than the
melting points of the individual components
EMLA = lidocaine and prilocaine become an oily
mixture.
EMLA cream is used to numb normal intact skin or the
membrane surfaces.
 Rules:

2% lidocaine :
2 grams of lidocaine 2000 mg of lidocaine
100 ml of solution 100 ml of solution
20 mg of lidocaine
1 ml of solution

1 ml of solution 20 mg lidocaine
1.8 ml of solution ??? mg lidocaine

=1.8 x 20= 36 mg lidocaine

Maximum dose of a 2% lidocaine solution is (300mg):
4.4 mg/kg body weight
In 70 kg adult patient would be:
70 x 4.4 = 308 mg of lidocaine
36 mg 1 cartridge
308 mg ??? Cartridges

308 / 36 = 8.5 cartridges

 Dosages

Anesthetic Max. dose Max. dose Max. dose Max. dose Max. dose
solution (mg/kg) of 1.8 ml of 1.8 ml of 2.2 ml of 2.2 ml
[absolute cartridges in cartridges in a cartridges in cartridges in a
ceiling an adult of 5-year-old an adult of 5-year-old
(mg)] 70 kg child of 20kg 70 kg child of 20kg

2% lignocaine 4.4 [300] 8.3 2.4 6.8 2

2% mepivacaine 4.4 [300] 8.3 2.4 6.8 2

3% mepivacaine 4.4 [300] 5.6 1.6 4.5 1.3

3% prilocaine 6.0 [400] 7.4 2.2 6 1.8

4% prilocaine 6.0 [600] 5.5 1.7 4.5 1.4

 Systemic action of LA
CNS

Their Pharmacological action on the CNS is depression

(toxic overdose).

Anticonvulsant properties.

Analgsia: IV administration increase pain threshold and

produce a degree of analgesia.

Mood Elevation cocaine.

 Systemic action of LA
CVS

More resistant than CNS

Direct action on the myocardium, various phases of
myocardium depolarization are reduced.
 Action of LA

Reversibly block action potential in all excitable

membranes
CVS and CNS are especially susceptible to their
actions.
Effect is related to their blood or plasma level
Blood level depends on, Rate of uptake, rate of
distribution in tissue, and biotransformation (liver) .
1
2
Factors considered when selecting L.A

-The duration of planned treatment

-any medical contraindication
-possible need for hemostasis
Armamentarium

Syringe

Needle

cartridge
I. Syringe:
It is the vehicle whereby the contents of the
anesthetic cartridge are delivered through the needle
to the patient.
Four types:
1. Non-disposable syringes:
a) Breech-loading , metallic , cartridge-type , aspirating.
b) Breech-loading , metallic , cartridge-type , self-
aspirating.
c) Breech-loading , plastic , cartridge-type , aspirating.
d) Pressure syringe for periodontal ligament injection
e) Jet injector (needle-less syringe).
2. Disposable Syringe
3. Safety syringe
3. Computer-controlled local anesthetic delivery
system.
Syringe components:

1. needle adapter
2. piston with harpoon
3. syringe barrel
4. finger grip
5. thumb ring
II. Needle

Needle is vehicle that permits local anesthetic

solution to travel from the dental cartridge into
the tissues surrounding the needle tip.
Most needles used in dentistry are stainless-steel
and disposable.
Parts of Needle

Bevel
Shaft
Hub
Syringe adaptor
Cartridge penetration end
Gauge
Gauge refers the diameter of the lumen of the needle:
the smaller the number , the greater the diameter of the
lumen
A 30-gauge needle has a smaller internal diameter than
25-gauge needle.
There is a growing trend toward the use of smaller
diameter needles based on the assumption that they are
less traumatic to the patient than needles with larger
diameter.
The most commonly used needles in dentistry are 30
gauge short and 27-gauge long.
 Length
Dental needles are available in three lengths;
Cartridge
Is a glass cylinder containing the local anesthetic
drug .
parts of dental cartridge:-
Aluminum cap.
Diaphragm.
Stopper.
cylindrical glass tube.
 Components of L.A Cartridge

L.A agent
Vasoconstrictor
Antioxidant/reducing agent
Preservative/bacteriostatic
Ringer’s solution.
fungicidal
Vasoconstrictors

Two types:
Sympathomimetic naturally occurring, epinephrine.
Synthetic polypeptides, Felypressin
 Clinical applications of epinephrine

Management of acute allergic reaction.

Management of bronchospasm.
Treatment of cardiac arrest.
As a vasoconstrictor for hemostasis.
As vasoconstrictor in LA to decrease absorption into CVS.
As vasoconstrictor in LA to increase duration of action.
To produce mydriasis.
 Epinephrine: (Adrenaline)
Uses in dentistry:

Local anaesthetic solution.

Gingival retraction cords.
In the ER as life-saving drug in anaphylaxis.

Mechanism of action:
Interact with adrenergic receptors in the
vessels
α1 & α2 producing vasoconstriction in skin
&mucus membranes.
β2 stimulation causing vasodilatation in
skeletal muscles.

Activation of beta receptors lead to

bronchodilation and cardiac stimulation
Metabolism:
Appears very rapidly in the systemic
circulation
Exogenously administered epinephrine is
metabolized extraneuronal and 1% is
excreted in the urine unchanged.
Dosage:
1:80,000 is the commonest dose used,
0.0125 mg/ml
12.5 µg/ml
Ratio:

Epinephrine is added to local anesthetics in

extremely dilute concentrations, best expressed as:
a ratio of grams of a drug: total ml of solution.
A 1:1000 preparation of epinephrine would be:
1 gram epinephrine 1000 mg epinephrine
1000 ml solution 1000 ml solution

1 mg epinephrine
1ml solution
Therefore, a 1: 80,000 of epinephrine would be:
1 gram epinephrine 1000 mg epinephrine
80,000 ml solution 80,000 ml solution
1 mg epinephrine
80 ml solution
Dosage

Normal healthy patient:

0.2 mg per appointment

10 ml of 1:50,000 dilution ( 5 cartridges )

20 ml of 1:100,000 dilution ( 11 cartridges )
40 ml of 1:200,000 dilution ( 22 cartridges )
Patient with clinically significant cardiovascular
disease ( ASA III/IV ):
0.04 mg per appointment

2 ml of 1:50,000 dilution (1 cartridge )

4 ml of 1: 100,000 dilution ( 2 cartridges )
8 ml of 1: 200,000 dilution ( 4 cartridges )
 Systemic effect:
Being a naturally occurring hormone, it exert a number of
physiological responses on the different systems.

The heart:

Has direct and indirect action:

o Direct action on β1 receptors increases the rate and
force of contraction raising cardiac output.
o Indirect action, increase pulse and cardiac output,
lead to rise in systolic blood pressure, (not with
dental dose)
Blood vessels:

Contain α1, α2 and β2 adrenoreceptors in the vessels

of the skin, mucous membrane and skeletal muscles.

o Action on α1 receptors causes vasoconstriction

since they are susceptible to endogenous nor-
epinephrine and exogenous epinephrine. Reduce
operative bleeding

o α2 receptors are only susceptible to circulating

epinephrine.
 β2 found in the skeletal muscles, and very uncommon
in the skin and mucous membrane, β2 stimulation
result in vasodilatation, lowering peripheral resistance
and a fall in the diastolic blood pressure. (with dental
dose)
Haemostasis:
The vasoconstricting effect.
Adrenaline promote platelets aggregation in the early
stages.
Fibrinolytic activity compromise clot stability.

Lungs:
Stimulation of β2 receptors in the lung lead to bronchial
muscle relaxation, life-saving in bronchial (spasm)
constriction during anaphylactic reaction.

Wound healing:
Reduced local tissue oxygen tension.
Epinephrine-induced fibrinolysis.
Felypressin:
It is an analogue of the naturally occurring Vasopressin.
Bind to vasopressin V1 receptor in the vascular smooth
muscle producing vasoconstriction and reduce local blood
flow.
Commonly used with 3% prilocane
Less potent than the catecholamines
poorer control of bleeding during operative procedures.
Acts on the venous side rather than the arterial side.
anti diuretic and oxytocic actions, the latter
contraindicating its use in pregnant pts

Dose:
0.03 IU/ml (0.54 µg/ml)
 Functions of vasoconstrictor in L.A

1. Decrease the rate of absorption of L.A so lessen the chance

of toxicity
2. Decrease blood flow ---Reduce bleeding tendency so it can
be used in GA.
3. Prolong the duration of L.A.
4. Localize the effect of LA---Produces profound anaesthesia.
 Reducing agent

vasoconstrictors are not stable in solution and may

be oxidized by prolong exposure to sunlight
leading to brown color discoloration so the
reducing agent e.g metabisulphide compete for
available oxygen result in stability.
 Preservative
1.stability
2.sterility of solution

E.g 1. caprylhydrocuprientoxin
2.methyl paraben which produce allergic reaction

Fungicide
thymol which prevent fungi proliferation and cloudy
solution.
 Vehicle

Ringer solution (plasma expander )

It reduces discomfort during

injection of L.A by plasma expansion
effect