About choline blockers pharma

1. 1
1
ANTICHOLINERGIC DRUGS
ANTICHOLINERGIC DRUGS
AND DRUGS ACTING ON AUTONOMIC
GANGLIA
AND DRUGS ACTING ON AUTONOMIC
GANGLIA
AND DRUGS ACTING ON AUTONOMIC
GANGLIA
Smolensk state medical
academy
Pharmacology department

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2
ANTICHOLINERGIC DRUGS (Muscarinic
receptor antagonists, Atropinics,
Parasympatholytics)
ANTICHOLINERGIC DRUGS (Muscarinic
receptor antagonists, Atropinics,
Parasympatholytics)
ANTICHOLINERGIC DRUGS (Muscarinic
receptor antagonists, Atropinics,
Parasympatholytics)
ANTICHOLINERGIC DRUGS (Muscarinic
receptor antagonists, Atropinics,
Parasympatholytics)


Conventionally, the term “anticholinergic
drugs” is restricted to those which block
actions of Ach on autonomic effectors
and in the CNS exerted through
muscarinic receptors.
Conventionally, the term “anticholinergic
drugs” is restricted to those which block
actions of Ach on autonomic effectors
and in the CNS exerted through
muscarinic receptors.
Conventionally, the term “anticholinergic
drugs” is restricted to those which block
actions of Ach on autonomic effectors
and in the CNS exerted through
muscarinic receptors.
Conventionally, the term “anticholinergic
drugs” is restricted to those which block
actions of Ach on autonomic effectors
and in the CNS exerted through
muscarinic receptors.
Conventionally, the term “anticholinergic
drugs” is restricted to those which block
actions of Ach on autonomic effectors
and in the CNS exerted through
muscarinic receptors.
Conventionally, the term “anticholinergic
drugs” is restricted to those which block
actions of Ach on autonomic effectors
and in the CNS exerted through
muscarinic receptors.
Though nicotinic receptor antagonists
also block certain actions of Ach, they are
generally reffered to as “ganglion blockers”
and “neuromuscular blockers.
Though nicotinic receptor antagonists
also block certain actions of Ach, they are
generally reffered to as “ganglion blockers”
and “neuromuscular blockers.
Though nicotinic receptor antagonists
also block certain actions of Ach, they are
generally reffered to as “ganglion blockers”
and “neuromuscular blockers.
Though nicotinic receptor antagonists
also block certain actions of Ach, they are
generally reffered to as “ganglion blockers”
and “neuromuscular blockers.
Though nicotinic receptor antagonists
also block certain actions of Ach, they are
generally reffered to as “ganglion blockers”
and “neuromuscular blockers.

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3
Classification of anticholinergic
drugs
Classification of anticholinergic
drugs
Classification of anticholinergic
drugs
1.
2.
3.


M, N - c h o l i n e r g i c b l o c k e r s
M, N - c h o l i n e r g i c b l o c k e r s
М – c h o l i n e r g i c b l o c k e r s
(antimuscarinic drugs)
М – c h o l i n e r g i c b l o c k e r s
(antimuscarinic drugs)
М – c h o l i n e r g i c b l o c k e r s
(antimuscarinic drugs)
N – c h o l i n e r g i c b l o c k e r s:
N – c h o l i n e r g i c b l o c k e r s:
Neuromuscular blocking agents
(skeletal muscle relaxant) - block Nm
receptor
Neuromuscular blocking agents
(skeletal muscle relaxant) - block Nm
receptor
Neuromuscular blocking agents
(skeletal muscle relaxant) - block Nm
receptor
Neuromuscular blocking agents
(skeletal muscle relaxant) - block Nm
receptor
Neuromuscular blocking agents
(skeletal muscle relaxant) - block Nm
receptor
Ganglion blockers - block Nn receptors
Ganglion blockers - block Nn receptors
Ganglion blockers - block Nn receptors

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4
Classification of cholinergic blockers
Classification of cholinergic blockers
ь
II.
ь
ь
ь
I. M, N - c h o l i n o b l o c k e r s:
I. M, N - c h o l i n o b l o c k e r s:
I. M, N - c h o l i n o b l o c k e r s:
Aprofene
Aprofene
М – c h o l i n o b l o c k e r s (Muscarinic
receptor antagonists, Atropinics):
М – c h o l i n o b l o c k e r s (Muscarinic
receptor antagonists, Atropinics):
М – c h o l i n o b l o c k e r s (Muscarinic
receptor antagonists, Atropinics):
1. Natural alkaloids
1. Natural alkaloids
1. Natural alkaloids
Atropine sulfate
Atropine sulfate
Hyoscine hydrobromide (Scopolamine)
Hyoscine hydrobromide (Scopolamine)
Platyphylline hydrotartrate
Platyphylline hydrotartrate
Platyphylline hydrotartrate

5. Muscarinic receptor antagonists
Muscarinic receptor antagonists
ь
ь
ь
ь
ь
2. Semisynthetic derivatives
2. Semisynthetic derivatives
Homatropine hydrobromide
Homatropine hydrobromide
Homatropine hydrobromide
Atropine methonitrate
Atropine methonitrate
Hyoscine butyl bromide
Hyoscine butyl bromide
Hyoscine butyl bromide
Ipratropium bromide (atrovent)
Ipratropium bromide (atrovent)
Tiotropium bromide
Tiotropium bromide
5
5

6. Muscarinic receptor antagonists
Muscarinic receptor antagonists


3. Synthetic compounds
3. Synthetic compounds
Mydriatics: Cyclopentolate, Tropicamide
Mydriatics: Cyclopentolate, Tropicamide
Mydriatics: Cyclopentolate, Tropicamide
Mydriatics: Cyclopentolate, Tropicamide
Mydriatics: Cyclopentolate, Tropicamide
Antisecretory-antispasmodics:
Antisecretory-antispasmodics:
Quaternary compounds: Propantheline,
Oxyphenonium, Clidinium, Pipenzolate
methylbromide, Isopropamide, Glycopyrrolate
Quaternary compounds: Propantheline,
Oxyphenonium, Clidinium, Pipenzolate
methylbromide, Isopropamide, Glycopyrrolate
Quaternary compounds: Propantheline,
Oxyphenonium, Clidinium, Pipenzolate
methylbromide, Isopropamide, Glycopyrrolate
Quaternary compounds: Propantheline,
Oxyphenonium, Clidinium, Pipenzolate
methylbromide, Isopropamide, Glycopyrrolate
Quaternary compounds: Propantheline,
Oxyphenonium, Clidinium, Pipenzolate
methylbromide, Isopropamide, Glycopyrrolate
Tertiary amines: Dicyclomine, Valethamate,
Pirenzepine
Tertiary amines: Dicyclomine, Valethamate,
Pirenzepine
Tertiary amines: Dicyclomine, Valethamate,
Pirenzepine
Tertiary amines: Dicyclomine, Valethamate,
Pirenzepine
6
6

7. Muscarinic receptor antagonists
Muscarinic receptor antagonists


Vasicoselective: Oxybutinine, Flavoxate,
Tolterodine
Vasicoselective: Oxybutinine, Flavoxate,
Tolterodine
Vasicoselective: Oxybutinine, Flavoxate,
Tolterodine
Vasicoselective: Oxybutinine, Flavoxate,
Tolterodine
Vasicoselective: Oxybutinine, Flavoxate,
Tolterodine
Antiparkinsonian: Trihexyphenidyl,
Procyclidine, Biperiden
Antiparkinsonian: Trihexyphenidyl,
Procyclidine, Biperiden
Antiparkinsonian: Trihexyphenidyl,
Procyclidine, Biperiden
Antiparkinsonian: Trihexyphenidyl,
Procyclidine, Biperiden
Antiparkinsonian: Trihexyphenidyl,
Procyclidine, Biperiden
7
7

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8
Classification of anticholinergic drugs
Classification of anticholinergic drugs
Ш

N – c h o l i n o b l o c k e r s
N – c h o l i n o b l o c k e r s
I. Neuromuscular blockers(skeletal muscle
relaxants)
I. Neuromuscular blockers(skeletal muscle
relaxants)
I. Neuromuscular blockers(skeletal muscle
relaxants)
I. Neuromuscular blockers(skeletal muscle
relaxants)
Depolarizing ones
Depolarizing ones
Depolarizing ones
Short-term acting (5-10 min)
Short-term acting (5-10 min)
Suxamethonium cloride
Suxamethonium cloride

9. Neuromuscular blocking agents
(skeletal muscle relaxants)
Neuromuscular blocking agents
(skeletal muscle relaxants)
Neuromuscular blocking agents
(skeletal muscle relaxants)








Non-depolarizing (anti-depolarizing) muscle
relaxant of competitive type action
Non-depolarizing (anti-depolarizing) muscle
relaxant of competitive type action
Non-depolarizing (anti-depolarizing) muscle
relaxant of competitive type action
Short-term acting (15-20 min)
Short-term acting (15-20 min)
Mivacurium chloride
Mivacurium chloride
Mid-term acting (30-60 min):
Mid-term acting (30-60 min):
Alcuronium chloride
Alcuronium chloride
Atracurium besilate
Atracurium besilate
Vecuronium bromide
Vecuronium bromide
Vecuronium bromide
Cisatracirium besilate
Cisatracirium besilate
Rocuronium bromide
Rocuronium bromide
9
9

10. Neuromuscular blocking agents
(skeletal muscle relaxants)
Neuromuscular blocking agents
(skeletal muscle relaxants)
Neuromuscular blocking agents
(skeletal muscle relaxants)







Long-term acting (60-120 min)
Long-term acting (60-120 min)
Pancuronium bromide
Pancuronium bromide
Pipecuronium bromide
Pipecuronium bromide
Pipecuronium bromide
Tubocurarine chloride
Tubocurarine chloride
Mellictinum
Mellictinum
Doxacurium
Doxacurium
Muscle relaxants of mixed action
Muscle relaxants of mixed action
Dioxonium
Dioxonium
10
10

11. 11
11
Classification of anticholinergic
drugs
Classification of anticholinergic
drugs
Classification of anticholinergic
drugs










Ganglion blockers (block Nn receptors):
Ganglion blockers (block Nn receptors):
Ganglion blockers (block Nn receptors):
Short-term acting ones (10-20 min)
Short-term acting ones (10-20 min)
Short-term acting ones (10-20 min)
Short-term acting ones (10-20 min)
Short-term acting ones (10-20 min)
Short-term acting ones (10-20 min)
Trepirium iodide
Trepirium iodide
Imechinum
Imechinum
Mid-term acting ones (3-4 hours)
Mid-term acting ones (3-4 hours)
Azamethonium bromide
Azamethonium bromide
Hexamethonium benzosulfonate (benzohexonium)
Hexamethonium benzosulfonate (benzohexonium)
Pachycarpine hydroiodide
Pachycarpine hydroiodide
Long-term acting ones (8 hours and more)
Long-term acting ones (8 hours and more)
Long-term acting ones (8 hours and more)
Pempidine tosylate
Pempidine tosylate
Temechinum
Temechinum

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М-cholinoreceptors
М-cholinoreceptors


Block М-cholinoceptors and prevent from
Асh action
Block М-cholinoceptors and prevent from
Асh action
Block М-cholinoceptors and prevent from
Асh action
Inhibit activity of parasympathetic nervous
system
Inhibit activity of parasympathetic nervous
system
Inhibit activity of parasympathetic nervous
system

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The main pharmacological effects:
The main pharmacological effects:
of М-cholinoblockers
of М-cholinoblockers









Influence on eye function:
Influence on eye function:
Influence on eye function:
as opposed to M-cholinomimetics:
as opposed to M-cholinomimetics:
as opposed to M-cholinomimetics:
as opposed to M-cholinomimetics:
as opposed to M-cholinomimetics:
dilate pupil (midriasis)
dilate pupil (midriasis)
dilate pupil (midriasis)
dilate pupil (midriasis)
paralyse (relax) accommodation
paralyse (relax) accommodation
increase intraocular tension
increase intraocular tension
Influence on smooth muscles:
Influence on smooth muscles:
Influence on smooth muscles:
decrease tone of smooth muscles of GIT, bronchi, biliary
and urinary tract
decrease tone of smooth muscles of GIT, bronchi, biliary
and urinary tract
decrease tone of smooth muscles of GIT, bronchi, biliary
and urinary tract
decrease tone of smooth muscles of GIT, bronchi, biliary
and urinary tract
decrease tone of smooth muscles of GIT, bronchi, biliary
and urinary tract
decrease tone of smooth muscles of GIT, bronchi, biliary
and urinary tract
decrease tone of smooth muscles of GIT, bronchi, biliary
and urinary tract
decrease tone of smooth muscles of GIT, bronchi, biliary
and urinary tract
Action on the heart:
Action on the heart:
tachycardia
tachycardia
tachycardia
increase in atrio-ventricular conduction and myocardium
oxygen demand
increase in atrio-ventricular conduction and myocardium
oxygen demand
increase in atrio-ventricular conduction and myocardium
oxygen demand

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14
The main pharmacological effects:
The main pharmacological effects:
of М-cholinoblockers
of М-cholinoblockers




Influence on gland secretion :
Influence on gland secretion :
Influence on gland secretion :
the drugs inhibit secretion of glands due to block
of М3-cholinoceptors of glandular cell
membranes
the drugs inhibit secretion of glands due to block
of М3-cholinoceptors of glandular cell
membranes
the drugs inhibit secretion of glands due to block
of М3-cholinoceptors of glandular cell
membranes
the drugs inhibit secretion of glands due to block
of М3-cholinoceptors of glandular cell
membranes
the drugs inhibit secretion of glands due to block
of М3-cholinoceptors of glandular cell
membranes
the drugs inhibit secretion of glands due to block
of М3-cholinoceptors of glandular cell
membranes
the drugs inhibit secretion of glands due to block
of М3-cholinoceptors of glandular cell
membranes
the drugs inhibit secretion of glands due to block
of М3-cholinoceptors of glandular cell
membranes
Secretion of salivary, nasopharyngeal, bronchial,
gastric, sweet and lachrymal glands decreases
Secretion of salivary, nasopharyngeal, bronchial,
gastric, sweet and lachrymal glands decreases
Secretion of salivary, nasopharyngeal, bronchial,
gastric, sweet and lachrymal glands decreases
Secretion of salivary, nasopharyngeal, bronchial,
gastric, sweet and lachrymal glands decreases
Secretion of salivary, nasopharyngeal, bronchial,
gastric, sweet and lachrymal glands decreases
That leads to dryness of the skin and mucous
membranes
That leads to dryness of the skin and mucous
membranes
That leads to dryness of the skin and mucous
membranes
That leads to dryness of the skin and mucous
membranes

15. The main pharmacological effects:
The main pharmacological effects:
of М-cholinoblockers
of М-cholinoblockers





Influence on thermoregulation
Influence on thermoregulation
Block М3-cholinoreceptors of sweet glands,
inhibit sweet secretion what can lead to
thermoregulation disturbance. As a result, body
temperature can increase.
Block М3-cholinoreceptors of sweet glands,
inhibit sweet secretion what can lead to
thermoregulation disturbance. As a result, body
temperature can increase.
Block М3-cholinoreceptors of sweet glands,
inhibit sweet secretion what can lead to
thermoregulation disturbance. As a result, body
temperature can increase.
Block М3-cholinoreceptors of sweet glands,
inhibit sweet secretion what can lead to
thermoregulation disturbance. As a result, body
temperature can increase.
Block М3-cholinoreceptors of sweet glands,
inhibit sweet secretion what can lead to
thermoregulation disturbance. As a result, body
temperature can increase.
Block М3-cholinoreceptors of sweet glands,
inhibit sweet secretion what can lead to
thermoregulation disturbance. As a result, body
temperature can increase.
Block М3-cholinoreceptors of sweet glands,
inhibit sweet secretion what can lead to
thermoregulation disturbance. As a result, body
temperature can increase.
Block М3-cholinoreceptors of sweet glands,
inhibit sweet secretion what can lead to
thermoregulation disturbance. As a result, body
temperature can increase.
Block М3-cholinoreceptors of sweet glands,
inhibit sweet secretion what can lead to
thermoregulation disturbance. As a result, body
temperature can increase.
Influence on the CNS
Influence on the CNS
Preparations of tertiary structure (Atropine,
Hyosyamine, Platyphyllin) pass through blood-
brain barrier and take action on the CNS.
Preparations of tertiary structure (Atropine,
Hyosyamine, Platyphyllin) pass through blood-
brain barrier and take action on the CNS.
Preparations of tertiary structure (Atropine,
Hyosyamine, Platyphyllin) pass through blood-
brain barrier and take action on the CNS.
Preparations of tertiary structure (Atropine,
Hyosyamine, Platyphyllin) pass through blood-
brain barrier and take action on the CNS.
Preparations of tertiary structure (Atropine,
Hyosyamine, Platyphyllin) pass through blood-
brain barrier and take action on the CNS.
Preparations of tertiary structure (Atropine,
Hyosyamine, Platyphyllin) pass through blood-
brain barrier and take action on the CNS.
Preparations of tertiary structure (Atropine,
Hyosyamine, Platyphyllin) pass through blood-
brain barrier and take action on the CNS.
Preparations of tertiary structure (Atropine,
Hyosyamine, Platyphyllin) pass through blood-
brain barrier and take action on the CNS.
Preparations of tertiary structure (Atropine,
Hyosyamine, Platyphyllin) pass through blood-
brain barrier and take action on the CNS.
Preparations of tertiary structure (Atropine,
Hyosyamine, Platyphyllin) pass through blood-
brain barrier and take action on the CNS.
At medium therapeutic dose Atropine blocks the
relative cholinergic overactivity of basal ganglia,
suppresses tremor and rigidity at parkinsonism.
At medium therapeutic dose Atropine blocks the
relative cholinergic overactivity of basal ganglia,
suppresses tremor and rigidity at parkinsonism.
At medium therapeutic dose Atropine blocks the
relative cholinergic overactivity of basal ganglia,
suppresses tremor and rigidity at parkinsonism.
At medium therapeutic dose Atropine blocks the
relative cholinergic overactivity of basal ganglia,
suppresses tremor and rigidity at parkinsonism. 15
15

16. 16
16
Comparative characteristics of
Comparative characteristics of
М-cholinoblockers
М-cholinoblockers







Atropine
Atropine
is an alkaloid contained in belladonna, black henbane,
datura (thornapple, mad apple)
is an alkaloid contained in belladonna, black henbane,
datura (thornapple, mad apple)
is an alkaloid contained in belladonna, black henbane,
datura (thornapple, mad apple)
is an alkaloid contained in belladonna, black henbane,
datura (thornapple, mad apple)
is an alkaloid contained in belladonna, black henbane,
datura (thornapple, mad apple)
is an alkaloid contained in belladonna, black henbane,
datura (thornapple, mad apple)
is an alkaloid contained in belladonna, black henbane,
datura (thornapple, mad apple)
is an alkaloid contained in belladonna, black henbane,
datura (thornapple, mad apple)
is an alkaloid contained in belladonna, black henbane,
datura (thornapple, mad apple)
is an alkaloid contained in belladonna, black henbane,
datura (thornapple, mad apple)
It is well absorbed from GIT and from mucous
membranes
It is well absorbed from GIT and from mucous
membranes
It is well absorbed from GIT and from mucous
membranes
Duration of resorptive effect is about 6 hours
Duration of resorptive effect is about 6 hours
Its biotransformation occurs in the liver
Its biotransformation occurs in the liver
it is mainly eliminated by kidney
it is mainly eliminated by kidney
It is non-selective blocker of М-cholinoceptors
It is non-selective blocker of М-cholinoceptors
At therapeutic doses it stimulates respiratory, vagal,
vasomotor medullary centers
At therapeutic doses it stimulates respiratory, vagal,
vasomotor medullary centers
At therapeutic doses it stimulates respiratory, vagal,
vasomotor medullary centers

17. Belladonna
Belladonna
17
17

18. Black henbane
Black henbane
18
18

19. DATURA STRAMONIUM
DATURA STRAMONIUM
19
19

20. Atropine
Atropine
 High doses cause cortical excitation,
restlessness, disorientation,
hallucinations and delirium, followed by
respiratory depression and coma.
High doses cause cortical excitation,
restlessness, disorientation,
hallucinations and delirium, followed by
respiratory depression and coma.
High doses cause cortical excitation,
restlessness, disorientation,
hallucinations and delirium, followed by
respiratory depression and coma.
High doses cause cortical excitation,
restlessness, disorientation,
hallucinations and delirium, followed by
respiratory depression and coma.
High doses cause cortical excitation,
restlessness, disorientation,
hallucinations and delirium, followed by
respiratory depression and coma.
20
20

21. 21
21
Comparative characteristics of
Comparative characteristics of
М-cholinoblockers
М-cholinoblockers






Platyphyllin
Platyphyllin
alkaloid, contained in plant groundsel
alkaloid, contained in plant groundsel
It has “double” spasmolytic action:
It has “double” spasmolytic action:
blocks м-cholinoreceptors, i.е. takes neurotropic
spasmolytic action
blocks м-cholinoreceptors, i.е. takes neurotropic
spasmolytic action
blocks м-cholinoreceptors, i.е. takes neurotropic
spasmolytic action
in contrast to other М-cholinoblockers it takes direct
myotropic spasmolytic action
in contrast to other М-cholinoblockers it takes direct
myotropic spasmolytic action
in contrast to other М-cholinoblockers it takes direct
myotropic spasmolytic action
Scopolamine
Scopolamine
It is characterized by high activity regarding М-
cholinoceptors of vestibular apparatus (antimotion
sickness property due to depression of vestibular
excitation)
It is characterized by high activity regarding М-
cholinoceptors of vestibular apparatus (antimotion
sickness property due to depression of vestibular
excitation)
It is characterized by high activity regarding М-
cholinoceptors of vestibular apparatus (antimotion
sickness property due to depression of vestibular
excitation)
It is characterized by high activity regarding М-
cholinoceptors of vestibular apparatus (antimotion
sickness property due to depression of vestibular
excitation)
It is characterized by high activity regarding М-
cholinoceptors of vestibular apparatus (antimotion
sickness property due to depression of vestibular
excitation)
It takes depressant and amnestic action on the CNS,
induces “twilight sleep” ans has been used as a lie
detector or truth serum
It takes depressant and amnestic action on the CNS,
induces “twilight sleep” ans has been used as a lie
detector or truth serum
It takes depressant and amnestic action on the CNS,
induces “twilight sleep” ans has been used as a lie
detector or truth serum
It takes depressant and amnestic action on the CNS,
induces “twilight sleep” ans has been used as a lie
detector or truth serum
It takes depressant and amnestic action on the CNS,
induces “twilight sleep” ans has been used as a lie
detector or truth serum

22. Senecio (groundsel)
Senecio (groundsel)
22
22

23. 23
23
Сomparative characteristics of
Сomparative characteristics of
М-cholinoblockers
М-cholinoblockers



Pirenzepine, Telenzepine
Pirenzepine, Telenzepine
Act selectively on М1-cholinoreceptors of the
stomach and inhibit gastric gland secretion of
hydrochloric acid and pepsinogen
Act selectively on М1-cholinoreceptors of the
stomach and inhibit gastric gland secretion of
hydrochloric acid and pepsinogen
Act selectively on М1-cholinoreceptors of the
stomach and inhibit gastric gland secretion of
hydrochloric acid and pepsinogen
Act selectively on М1-cholinoreceptors of the
stomach and inhibit gastric gland secretion of
hydrochloric acid and pepsinogen
Act selectively on М1-cholinoreceptors of the
stomach and inhibit gastric gland secretion of
hydrochloric acid and pepsinogen
Act selectively on М1-cholinoreceptors of the
stomach and inhibit gastric gland secretion of
hydrochloric acid and pepsinogen
Ipratropium, Tiotropium
Ipratropium, Tiotropium
Are quaternary atropinics
Are quaternary atropinics
they more markedly block М-cholinoceptors of
smooth muscles of bronchi and cause their
dilation
they more markedly block М-cholinoceptors of
smooth muscles of bronchi and cause their
dilation
they more markedly block М-cholinoceptors of
smooth muscles of bronchi and cause their
dilation
they more markedly block М-cholinoceptors of
smooth muscles of bronchi and cause their
dilation

24. 24
24
Indication for administration of
Indication for administration of
М-cholinoblockers
М-cholinoblockers
1.
2.
3.
4.
5.
For preanaesthetic medication (Atropine, Glycopyrrolate)
. They is used to inhibit bronchial secretion, to block
vagal influence for prevention of reflex cardiac arrest
and respiratory standstill
For preanaesthetic medication (Atropine, Glycopyrrolate)
. They is used to inhibit bronchial secretion, to block
vagal influence for prevention of reflex cardiac arrest
and respiratory standstill
For preanaesthetic medication (Atropine, Glycopyrrolate)
. They is used to inhibit bronchial secretion, to block
vagal influence for prevention of reflex cardiac arrest
and respiratory standstill
For preanaesthetic medication (Atropine, Glycopyrrolate)
. They is used to inhibit bronchial secretion, to block
vagal influence for prevention of reflex cardiac arrest
and respiratory standstill
For preanaesthetic medication (Atropine, Glycopyrrolate)
. They is used to inhibit bronchial secretion, to block
vagal influence for prevention of reflex cardiac arrest
and respiratory standstill
For preanaesthetic medication (Atropine, Glycopyrrolate)
. They is used to inhibit bronchial secretion, to block
vagal influence for prevention of reflex cardiac arrest
and respiratory standstill
For preanaesthetic medication (Atropine, Glycopyrrolate)
. They is used to inhibit bronchial secretion, to block
vagal influence for prevention of reflex cardiac arrest
and respiratory standstill
For preanaesthetic medication (Atropine, Glycopyrrolate)
. They is used to inhibit bronchial secretion, to block
vagal influence for prevention of reflex cardiac arrest
and respiratory standstill
For preanaesthetic medication (Atropine, Glycopyrrolate)
. They is used to inhibit bronchial secretion, to block
vagal influence for prevention of reflex cardiac arrest
and respiratory standstill
For elimination of spasms of smooth muscles of GIT,
urinary tract , biliary tract more frequently Dicyclomine,
Valethamate, Pipenzolate)
For elimination of spasms of smooth muscles of GIT,
urinary tract , biliary tract more frequently Dicyclomine,
Valethamate, Pipenzolate)
For elimination of spasms of smooth muscles of GIT,
urinary tract , biliary tract more frequently Dicyclomine,
Valethamate, Pipenzolate)
For elimination of spasms of smooth muscles of GIT,
urinary tract , biliary tract more frequently Dicyclomine,
Valethamate, Pipenzolate)
For elimination of spasms of smooth muscles of GIT,
urinary tract , biliary tract more frequently Dicyclomine,
Valethamate, Pipenzolate)
For elimination of spasms of smooth muscles of GIT,
urinary tract , biliary tract more frequently Dicyclomine,
Valethamate, Pipenzolate)
For elimination of spasms of smooth muscles of GIT,
urinary tract , biliary tract more frequently Dicyclomine,
Valethamate, Pipenzolate)
For elimination of spasms of smooth muscles of GIT,
urinary tract , biliary tract more frequently Dicyclomine,
Valethamate, Pipenzolate)
For relief of bronchospasm in COPD and bronchial
asthma (Ipratropium, Tiotropium) by inhalation)
For relief of bronchospasm in COPD and bronchial
asthma (Ipratropium, Tiotropium) by inhalation)
For relief of bronchospasm in COPD and bronchial
asthma (Ipratropium, Tiotropium) by inhalation)
For relief of bronchospasm in COPD and bronchial
asthma (Ipratropium, Tiotropium) by inhalation)
For relief of bronchospasm in COPD and bronchial
asthma (Ipratropium, Tiotropium) by inhalation)
For relief of bronchospasm in COPD and bronchial
asthma (Ipratropium, Tiotropium) by inhalation)
For relief of bronchospasm in COPD and bronchial
asthma (Ipratropium, Tiotropium) by inhalation)
For relief of bronchospasm in COPD and bronchial
asthma (Ipratropium, Tiotropium) by inhalation)
Stomach ulcer, hyperacid gastritis to inhibit secretion
of HCl (Pirenzepine, Telenzepine, Propantheline)
Stomach ulcer, hyperacid gastritis to inhibit secretion
of HCl (Pirenzepine, Telenzepine, Propantheline)
Stomach ulcer, hyperacid gastritis to inhibit secretion
of HCl (Pirenzepine, Telenzepine, Propantheline)
Stomach ulcer, hyperacid gastritis to inhibit secretion
of HCl (Pirenzepine, Telenzepine, Propantheline)
Stomach ulcer, hyperacid gastritis to inhibit secretion
of HCl (Pirenzepine, Telenzepine, Propantheline)
Stomach ulcer, hyperacid gastritis to inhibit secretion
of HCl (Pirenzepine, Telenzepine, Propantheline)
Hyperkinesia, Parkinsonism (Trihexyphenidyl,
Procyclidine, Biperiden)
Hyperkinesia, Parkinsonism (Trihexyphenidyl,
Procyclidine, Biperiden)
Hyperkinesia, Parkinsonism (Trihexyphenidyl,
Procyclidine, Biperiden)
Hyperkinesia, Parkinsonism (Trihexyphenidyl,
Procyclidine, Biperiden)
Hyperkinesia, Parkinsonism (Trihexyphenidyl,
Procyclidine, Biperiden)
Hyperkinesia, Parkinsonism (Trihexyphenidyl,
Procyclidine, Biperiden)
Hyperkinesia, Parkinsonism (Trihexyphenidyl,
Procyclidine, Biperiden)

25. 25
25
Indications for administration of
Indications for administration of
М-cholinoblockers
М-cholinoblockers




6. In ophthalmology
6. In ophthalmology
6. In ophthalmology
6. In ophthalmology
6. In ophthalmology
To dilate pupil for choice of eyeglasses, for
examination of eye fundus (Tropicamide,
Cyclopentholate, Homatropine)
To dilate pupil for choice of eyeglasses, for
examination of eye fundus (Tropicamide,
Cyclopentholate, Homatropine)
To dilate pupil for choice of eyeglasses, for
examination of eye fundus (Tropicamide,
Cyclopentholate, Homatropine)
To dilate pupil for choice of eyeglasses, for
examination of eye fundus (Tropicamide,
Cyclopentholate, Homatropine)
To dilate pupil for choice of eyeglasses, for
examination of eye fundus (Tropicamide,
Cyclopentholate, Homatropine)
eye trauma, iridocyclitis (due to paralysis of
accomodation and relaxation of circular muscle of eye
pain decreases and healing is accelerated (Atropine)
eye trauma, iridocyclitis (due to paralysis of
accomodation and relaxation of circular muscle of eye
pain decreases and healing is accelerated (Atropine)
eye trauma, iridocyclitis (due to paralysis of
accomodation and relaxation of circular muscle of eye
pain decreases and healing is accelerated (Atropine)
eye trauma, iridocyclitis (due to paralysis of
accomodation and relaxation of circular muscle of eye
pain decreases and healing is accelerated (Atropine)
eye trauma, iridocyclitis (due to paralysis of
accomodation and relaxation of circular muscle of eye
pain decreases and healing is accelerated (Atropine)
eye trauma, iridocyclitis (due to paralysis of
accomodation and relaxation of circular muscle of eye
pain decreases and healing is accelerated (Atropine)
eye trauma, iridocyclitis (due to paralysis of
accomodation and relaxation of circular muscle of eye
pain decreases and healing is accelerated (Atropine)
eye trauma, iridocyclitis (due to paralysis of
accomodation and relaxation of circular muscle of eye
pain decreases and healing is accelerated (Atropine)
eye trauma, iridocyclitis (due to paralysis of
accomodation and relaxation of circular muscle of eye
pain decreases and healing is accelerated (Atropine)
7. Naupathia (motion sickness) – occurs in excitation of
М-cholinoreceptors of vestibular apparatus
(Scopolamine)
7. Naupathia (motion sickness) – occurs in excitation of
М-cholinoreceptors of vestibular apparatus
(Scopolamine)
7. Naupathia (motion sickness) – occurs in excitation of
М-cholinoreceptors of vestibular apparatus
(Scopolamine)
7. Naupathia (motion sickness) – occurs in excitation of
М-cholinoreceptors of vestibular apparatus
(Scopolamine)
7. Naupathia (motion sickness) – occurs in excitation of
М-cholinoreceptors of vestibular apparatus
(Scopolamine)
7. Naupathia (motion sickness) – occurs in excitation of
М-cholinoreceptors of vestibular apparatus
(Scopolamine)
7. Naupathia (motion sickness) – occurs in excitation of
М-cholinoreceptors of vestibular apparatus
(Scopolamine)
7. Naupathia (motion sickness) – occurs in excitation of
М-cholinoreceptors of vestibular apparatus
(Scopolamine)
7. Naupathia (motion sickness) – occurs in excitation of
М-cholinoreceptors of vestibular apparatus
(Scopolamine)
8. Poisoning with M-cholinomimetics and and
anticholinesterases (Atropine)
8. Poisoning with M-cholinomimetics and and
anticholinesterases (Atropine)
8. Poisoning with M-cholinomimetics and and
anticholinesterases (Atropine)
8. Poisoning with M-cholinomimetics and and
anticholinesterases (Atropine)
8. Poisoning with M-cholinomimetics and and
anticholinesterases (Atropine)
8. Poisoning with M-cholinomimetics and and
anticholinesterases (Atropine)
9. In cardiology
9. In cardiology
9. In cardiology
9. In cardiology
Vagal cardiac arrhythmia
Vagal cardiac arrhythmia
Atrioventricular block (Atropine, synthetic analogues)
Atrioventricular block (Atropine, synthetic analogues)
Atrioventricular block (Atropine, synthetic analogues)

26. Indications for administration of
Indications for administration of
М-cholinoblockers
М-cholinoblockers


10. In urology (vasicoselective drugs)
10. In urology (vasicoselective drugs)
10. In urology (vasicoselective drugs)
10. In urology (vasicoselective drugs)
For treatment of urinary incontinence
(detrusor instability)
For treatment of urinary incontinence
(detrusor instability)
For treatment of urinary incontinence
(detrusor instability)
renal colics (Oxybutinin, Dicyclomine,
Flavoxate)
renal colics (Oxybutinin, Dicyclomine,
Flavoxate)
renal colics (Oxybutinin, Dicyclomine,
Flavoxate)
renal colics (Oxybutinin, Dicyclomine,
Flavoxate)
26
26

27. 27
27
Adverse effects of
Adverse effects of
М-cholinoblockers
М-cholinoblockers






dry mouth
dry mouth
dysphagia, speech disturbance (dysarthria)
dysphagia, speech disturbance (dysarthria)
accomodation disorders
accomodation disorders
tachycardia
tachycardia
constipation
constipation
urinary retention
urinary retention

28. 28
28
Poisoning by atropine and atropinics
Poisoning by atropine and atropinics









Clinical symptoms of acute poisonning:
Clinical symptoms of acute poisonning:
dry flushed and hot skin, especially over face and neck
dry flushed and hot skin, especially over face and neck
hyperthermia,
hyperthermia,
tachycardia, rapid («galloping») pulse,
tachycardia, rapid («galloping») pulse,
tachycardia, rapid («galloping») pulse,
tachycardia, rapid («galloping») pulse,
tachycardia, rapid («galloping») pulse,
tachycardia, rapid («galloping») pulse,
shining dilated pipils, accomodation paralysis (blurring
of near vision), diplopia, photophobia, intraocular
tension increase,
shining dilated pipils, accomodation paralysis (blurring
of near vision), diplopia, photophobia, intraocular
tension increase,
shining dilated pipils, accomodation paralysis (blurring
of near vision), diplopia, photophobia, intraocular
tension increase,
shining dilated pipils, accomodation paralysis (blurring
of near vision), diplopia, photophobia, intraocular
tension increase,
dyspnea (tachypnea),
dyspnea (tachypnea),
headache,
headache,
Dry mouth and throat, dysphagia, speech disturbance
(dysarthria)
Dry mouth and throat, dysphagia, speech disturbance
(dysarthria)
Dry mouth and throat, dysphagia, speech disturbance
(dysarthria)
Urinary retention,
Urinary retention,
Excitement, psychotic behaviour, ataxia, delirium,
dreadfull hallucinations
Excitement, psychotic behaviour, ataxia, delirium,
dreadfull hallucinations
Excitement, psychotic behaviour, ataxia, delirium,
dreadfull hallucinations

29. 29
29
Poisonning by atropine and its analogues
Poisonning by atropine and its analogues




in severe cases – convulsion with loss of
consciousness, coma, hypotension;
in severe cases – convulsion with loss of
consciousness, coma, hypotension;
in severe cases – convulsion with loss of
consciousness, coma, hypotension;
in severe cases – convulsion with loss of
consciousness, coma, hypotension;
in severe cases – convulsion with loss of
consciousness, coma, hypotension;
in severe cases – convulsion with loss of
consciousness, coma, hypotension;
in severe cases – convulsion with loss of
consciousness, coma, hypotension;
Phase of excitement can be absent in children,
Phase of excitement can be absent in children,
poisoning is more dangerous for children;
poisoning is more dangerous for children;
approximate lethal dose of atropine and
scopolamine for adults is more 100 мg, for children
less 10 years of age – about 10 мg
approximate lethal dose of atropine and
scopolamine for adults is more 100 мg, for children
less 10 years of age – about 10 мg
approximate lethal dose of atropine and
scopolamine for adults is more 100 мg, for children
less 10 years of age – about 10 мg
approximate lethal dose of atropine and
scopolamine for adults is more 100 мg, for children
less 10 years of age – about 10 мg

30. 30
30
Mesures of first aid in poisonning
Mesures of first aid in poisonning
1.


3.

Removal of non-absorbed poison from GIT
Removal of non-absorbed poison from GIT
gastric lavage with tannic acid, saline purgatives (MgSO4),
activated charcoal
gastric lavage with tannic acid, saline purgatives (MgSO4),
activated charcoal
gastric lavage with tannic acid, saline purgatives (MgSO4),
activated charcoal
2. “dilution” and elimination of poison from the blood
2. “dilution” and elimination of poison from the blood
2. “dilution” and elimination of poison from the blood
2. “dilution” and elimination of poison from the blood
2. “dilution” and elimination of poison from the blood
2. “dilution” and elimination of poison from the blood
2. “dilution” and elimination of poison from the blood
forced diuresis (i/v saline infusion+diuretic Furosemide)
forced diuresis (i/v saline infusion+diuretic Furosemide)
Administration of pharmacological antagonists:
anticholinesterases of reversible action
Administration of pharmacological antagonists:
anticholinesterases of reversible action
Administration of pharmacological antagonists:
anticholinesterases of reversible action
Physostigmine, Galantamine. They promote accumulation
of Асh, which displaces M-cholinoblockers from bond to
receptor
Physostigmine, Galantamine. They promote accumulation
of Асh, which displaces M-cholinoblockers from bond to
receptor
Physostigmine, Galantamine. They promote accumulation
of Асh, which displaces M-cholinoblockers from bond to
receptor
Physostigmine, Galantamine. They promote accumulation
of Асh, which displaces M-cholinoblockers from bond to
receptor
Physostigmine, Galantamine. They promote accumulation
of Асh, which displaces M-cholinoblockers from bond to
receptor
Physostigmine, Galantamine. They promote accumulation
of Асh, which displaces M-cholinoblockers from bond to
receptor
Physostigmine, Galantamine. They promote accumulation
of Асh, which displaces M-cholinoblockers from bond to
receptor
4. Symptomatic therapy: tranquilizers, sedatives; physical
cooling;
4. Symptomatic therapy: tranquilizers, sedatives; physical
cooling;
4. Symptomatic therapy: tranquilizers, sedatives; physical
cooling;
4. Symptomatic therapy: tranquilizers, sedatives; physical
cooling;
4. Symptomatic therapy: tranquilizers, sedatives; physical
cooling;
4. Symptomatic therapy: tranquilizers, sedatives; physical
cooling;
4. Symptomatic therapy: tranquilizers, sedatives; physical
cooling;
4. Symptomatic therapy: tranquilizers, sedatives; physical
cooling;
in respiratory impairments - artificial lung ventilation,
in respiratory impairments - artificial lung ventilation,
in tachycardia – β-adrenoblockers
in tachycardia – β-adrenoblockers

31. 31
31
Contraindications:
Contraindications:




glaucoma
glaucoma
myocardium lesion, heart valvular defect,
cardiac insufficiency
myocardium lesion, heart valvular defect,
cardiac insufficiency
myocardium lesion, heart valvular defect,
cardiac insufficiency
myocardium lesion, heart valvular defect,
cardiac insufficiency
myocardium lesion, heart valvular defect,
cardiac insufficiency
hyperthermia
hyperthermia
hypertension and tachycardia
hypertension and tachycardia

32. 32
32
N-cholinoblockers
N-cholinoblockers






block nicotinic receptor, as a result, they stop
transmission of nerve impulses in corresponding
synapses;
block nicotinic receptor, as a result, they stop
transmission of nerve impulses in corresponding
synapses;
block nicotinic receptor, as a result, they stop
transmission of nerve impulses in corresponding
synapses;
block nicotinic receptor, as a result, they stop
transmission of nerve impulses in corresponding
synapses;
block nicotinic receptor, as a result, they stop
transmission of nerve impulses in corresponding
synapses;
block nicotinic receptor, as a result, they stop
transmission of nerve impulses in corresponding
synapses;
N-cholinoceptors are not homogeneous and unequally
react to pharmacological analyzers;
N-cholinoceptors are not homogeneous and unequally
react to pharmacological analyzers;
N-cholinoceptors are not homogeneous and unequally
react to pharmacological analyzers;
N-cholinoceptors are not homogeneous and unequally
react to pharmacological analyzers;
N-cholinoceptors are not homogeneous and unequally
react to pharmacological analyzers;
N-cholinoceptors are not homogeneous and unequally
react to pharmacological analyzers;
N-cholinoceptors are not homogeneous and unequally
react to pharmacological analyzers;
N-cholinoceptors are not homogeneous and unequally
react to pharmacological analyzers;
thus, N-cholinoceptors of skeletal muscles are sensitive
to tubocurarin and not blocked by hexamethonium;
thus, N-cholinoceptors of skeletal muscles are sensitive
to tubocurarin and not blocked by hexamethonium;
thus, N-cholinoceptors of skeletal muscles are sensitive
to tubocurarin and not blocked by hexamethonium;
thus, N-cholinoceptors of skeletal muscles are sensitive
to tubocurarin and not blocked by hexamethonium;
thus, N-cholinoceptors of skeletal muscles are sensitive
to tubocurarin and not blocked by hexamethonium;
thus, N-cholinoceptors of skeletal muscles are sensitive
to tubocurarin and not blocked by hexamethonium;
thus, N-cholinoceptors of skeletal muscles are sensitive
to tubocurarin and not blocked by hexamethonium;
N-cholinoreceptors of vegetative ganglions, to the
contrary, are blocked by Hexamethonium and not
sensitive to tubocurarin;
N-cholinoreceptors of vegetative ganglions, to the
contrary, are blocked by Hexamethonium and not
sensitive to tubocurarin;
N-cholinoreceptors of vegetative ganglions, to the
contrary, are blocked by Hexamethonium and not
sensitive to tubocurarin;
N-cholinoreceptors of vegetative ganglions, to the
contrary, are blocked by Hexamethonium and not
sensitive to tubocurarin;
N-cholinoreceptors of vegetative ganglions, to the
contrary, are blocked by Hexamethonium and not
sensitive to tubocurarin;
N-cholinoreceptors of vegetative ganglions, to the
contrary, are blocked by Hexamethonium and not
sensitive to tubocurarin;
N-cholinoreceptors of vegetative ganglions, to the
contrary, are blocked by Hexamethonium and not
sensitive to tubocurarin;
so, nicotitinic receptors of skeletal muscles are
conditionally designated as Nm-cholinoceptors;
so, nicotitinic receptors of skeletal muscles are
conditionally designated as Nm-cholinoceptors;
so, nicotitinic receptors of skeletal muscles are
conditionally designated as Nm-cholinoceptors;
so, nicotitinic receptors of skeletal muscles are
conditionally designated as Nm-cholinoceptors;
so, nicotitinic receptors of skeletal muscles are
conditionally designated as Nm-cholinoceptors;
so, nicotitinic receptors of skeletal muscles are
conditionally designated as Nm-cholinoceptors;
so, nicotitinic receptors of skeletal muscles are
conditionally designated as Nm-cholinoceptors;
Receptors of vegetative ganglion neurones –
Receptors of vegetative ganglion neurones –
Receptors of vegetative ganglion neurones –
Nn-cholinoceptors
Nn-cholinoceptors
Nn-cholinoceptors

33. 33
33
N-cholinoblockers
N-cholinoblockers
ь
ь
According to selectivity of action on this
two types receptors preparations of N-
cholinoblockers are divided into 2 groups:
According to selectivity of action on this
two types receptors preparations of N-
cholinoblockers are divided into 2 groups:
According to selectivity of action on this
two types receptors preparations of N-
cholinoblockers are divided into 2 groups:
According to selectivity of action on this
two types receptors preparations of N-
cholinoblockers are divided into 2 groups:
Skeletal muscle relaxants
Skeletal muscle relaxants
(block Nm-cholinoceptors) and
(block Nm-cholinoceptors) and
(block Nm-cholinoceptors) and
(block Nm-cholinoceptors) and
(block Nm-cholinoceptors) and
Ganglion blockers
Ganglion blockers
Ganglion blockers
(block Nn-cholinoceptors)
(block Nn-cholinoceptors)

34. 34
34
Ganglion blockers
Ganglion blockers
 block Nn-cholinoceptors in autonomic
ganglia of sympathetic and
parasympathetic nervous system
block Nn-cholinoceptors in autonomic
ganglia of sympathetic and
parasympathetic nervous system
block Nn-cholinoceptors in autonomic
ganglia of sympathetic and
parasympathetic nervous system
block Nn-cholinoceptors in autonomic
ganglia of sympathetic and
parasympathetic nervous system

35. 35
35
Ganglionic blockers
Ganglionic blockers




Classification according to chemical structure:
Classification according to chemical structure:
Quaternary ammonium compounds:
Quaternary ammonium compounds:
Imechinum, Trepirium, Azamethonium,
Hexamethonium
Imechinum, Trepirium, Azamethonium,
Hexamethonium
Imechinum, Trepirium, Azamethonium,
Hexamethonium
Imechinum, Trepirium, Azamethonium,
Hexamethonium
Imechinum, Trepirium, Azamethonium,
Hexamethonium
Imechinum, Trepirium, Azamethonium,
Hexamethonium
Imechinum, Trepirium, Azamethonium,
Hexamethonium
they are badly absorbed from GIT
they are badly absorbed from GIT
they do not pass to the CNS
they do not pass to the CNS
Tertiary amines:
Tertiary amines:
Pachicarpine, Pempidine, Temechinum
Pachicarpine, Pempidine, Temechinum
Pachicarpine, Pempidine, Temechinum
they are absorbed from intestine
they are absorbed from intestine
they pass through blood-brain barrier
they pass through blood-brain barrier

36. 36
36
Ganglion blockers
Ganglion blockers
Classification according to duration of action:
Classification according to duration of action:










Short-term acting (10-20 min)
Short-term acting (10-20 min)
Short-term acting (10-20 min)
Short-term acting (10-20 min)
Short-term acting (10-20 min)
Trepirium iodide (Hygronium)
Trepirium iodide (Hygronium)
Trepirium iodide (Hygronium)
Imechinum
Imechinum
Used for controlled hypotension during operations to
decrease loss of blood
Used for controlled hypotension during operations to
decrease loss of blood
Used for controlled hypotension during operations to
decrease loss of blood
Mid-term acting (1-4 hours)
Mid-term acting (1-4 hours)
Mid-term acting (1-4 hours)
Azamethonium bromide
Azamethonium bromide
Azamethonium bromide
Hexamethonium benzosulfonate
Hexamethonium benzosulfonate
Pachicarpine hydroiodide
Pachicarpine hydroiodide
used for relief of hypertensic crysis
used for relief of hypertensic crysis
used for relief of hypertensic crysis
Long-term acting (6-12 hours)
Long-term acting (6-12 hours)
Long-term acting (6-12 hours)
Pempidine
Pempidine
Pempidine
Temechinum
Temechinum

37. 37
37
Mechanism of ganglionic blocker action
Mechanism of ganglionic blocker action



is related to block of Nn-cholinoceptors in
synapses of vegetative ganglia, medulla
of adrenals, sino-carotide zone
is related to block of Nn-cholinoceptors in
synapses of vegetative ganglia, medulla
of adrenals, sino-carotide zone
is related to block of Nn-cholinoceptors in
synapses of vegetative ganglia, medulla
of adrenals, sino-carotide zone
is related to block of Nn-cholinoceptors in
synapses of vegetative ganglia, medulla
of adrenals, sino-carotide zone
the preparations block receptors in
sympathetic and parasympathyic ganglia
differently
the preparations block receptors in
sympathetic and parasympathyic ganglia
differently
the preparations block receptors in
sympathetic and parasympathyic ganglia
differently
the preparations block receptors in
sympathetic and parasympathyic ganglia
differently
thus, Hexamethonium and Pempidine
block ion channels, coupled to Nn-
cholinoreceptors
thus, Hexamethonium and Pempidine
block ion channels, coupled to Nn-
cholinoreceptors
thus, Hexamethonium and Pempidine
block ion channels, coupled to Nn-
cholinoreceptors
thus, Hexamethonium and Pempidine
block ion channels, coupled to Nn-
cholinoreceptors
thus, Hexamethonium and Pempidine
block ion channels, coupled to Nn-
cholinoreceptors
thus, Hexamethonium and Pempidine
block ion channels, coupled to Nn-
cholinoreceptors
thus, Hexamethonium and Pempidine
block ion channels, coupled to Nn-
cholinoreceptors
thus, Hexamethonium and Pempidine
block ion channels, coupled to Nn-
cholinoreceptors

38. 38
38
Mechanism of ganglionic blocker action
Mechanism of ganglionic blocker action






other preparations (Imecninum) block
recognizing receptor sites
other preparations (Imecninum) block
recognizing receptor sites
other preparations (Imecninum) block
recognizing receptor sites
other preparations (Imecninum) block
recognizing receptor sites
other preparations (Imecninum) block
recognizing receptor sites
as a result, ganglion blockers interrupt impulse
transmission in ganglia
as a result, ganglion blockers interrupt impulse
transmission in ganglia
as a result, ganglion blockers interrupt impulse
transmission in ganglia
impulse flow to nerve endings stops
impulse flow to nerve endings stops
that results in a decrease of noradrenalin release
in synapses of vessels
that results in a decrease of noradrenalin release
in synapses of vessels
that results in a decrease of noradrenalin release
in synapses of vessels
adrenaline secretion in chromaffin cells of
adrenal glands decreases
adrenaline secretion in chromaffin cells of
adrenal glands decreases
adrenaline secretion in chromaffin cells of
adrenal glands decreases
block of parasympathetic ganglions leads to
stoppage of impulses to smooth muscles of GIT,
bronchi and glands.
block of parasympathetic ganglions leads to
stoppage of impulses to smooth muscles of GIT,
bronchi and glands.
block of parasympathetic ganglions leads to
stoppage of impulses to smooth muscles of GIT,
bronchi and glands.
block of parasympathetic ganglions leads to
stoppage of impulses to smooth muscles of GIT,
bronchi and glands.

39. 39
39
Pharmacological effects of ganglion
blockers
Pharmacological effects of ganglion
blockers
Pharmacological effects of ganglion
blockers






As a result of block of parasympathetic ganglia:
As a result of block of parasympathetic ganglia:
arteries, veins, peripheral blood vessels are
dilated,
arteries, veins, peripheral blood vessels are
dilated,
arteries, veins, peripheral blood vessels are
dilated,
ABP decrease,
ABP decrease,
t.p.r., pre- and afterload decrease,
t.p.r., pre- and afterload decrease,
tissue microcirculation is improved,
tissue microcirculation is improved,
blood congestion in veins increases
blood congestion in veins increases
uterine tone increases
uterine tone increases

40. 40
40
Pharmacological effects of ganglion
blockers
Pharmacological effects of ganglion
blockers
Pharmacological effects of ganglion
blockers



As a result of block of parasympathetic ganglia:
As a result of block of parasympathetic ganglia:
a tone and motility of smooth muscles decrease
a tone and motility of smooth muscles decrease
a tone and motility of smooth muscles decrease
secretion of salivary, gastric, bronchial glands
decrease
secretion of salivary, gastric, bronchial glands
decrease
secretion of salivary, gastric, bronchial glands
decrease
block of reflex reactions
block of reflex reactions
Nowadays ganglion blockers
Nowadays ganglion blockers
Nowadays ganglion blockers
are used very seldom, as their action is nonselective
and so they have many adverse effects
are used very seldom, as their action is nonselective
and so they have many adverse effects
are used very seldom, as their action is nonselective
and so they have many adverse effects

41. 41
41
Adverse effects of ganglion blockers
Adverse effects of ganglion blockers







Orthostatic collapse (fall of arterial blood
pressure)
Orthostatic collapse (fall of arterial blood
pressure)
Orthostatic collapse (fall of arterial blood
pressure)
Danger of thrombosis due to slowing-down of blood flow
(stasis)
Danger of thrombosis due to slowing-down of blood flow
(stasis)
Danger of thrombosis due to slowing-down of blood flow
(stasis)
Danger of thrombosis due to slowing-down of blood flow
(stasis)
To prevent orthostatic collapse ganglion blockers must
be injected in recumbent position and after introduction
patient must stay recumbent for 2 hours
To prevent orthostatic collapse ganglion blockers must
be injected in recumbent position and after introduction
patient must stay recumbent for 2 hours
To prevent orthostatic collapse ganglion blockers must
be injected in recumbent position and after introduction
patient must stay recumbent for 2 hours
To prevent orthostatic collapse ganglion blockers must
be injected in recumbent position and after introduction
patient must stay recumbent for 2 hours
To prevent orthostatic collapse ganglion blockers must
be injected in recumbent position and after introduction
patient must stay recumbent for 2 hours
To prevent orthostatic collapse ganglion blockers must
be injected in recumbent position and after introduction
patient must stay recumbent for 2 hours
Atony of intestine and urinary bladder,
Atony of intestine and urinary bladder,
Constipation, urinary retention,
Constipation, urinary retention,
Constipation, urinary retention,
Constipation, urinary retention,
Midriasis, paralysis of accomodation,
Midriasis, paralysis of accomodation,
Dry mouth, dysphagy, dysarthria (speech
disturbance)
Dry mouth, dysphagy, dysarthria (speech
disturbance)
Dry mouth, dysphagy, dysarthria (speech
disturbance)
Dry mouth, dysphagy, dysarthria (speech
disturbance)
Dry mouth, dysphagy, dysarthria (speech
disturbance)
Dry mouth, dysphagy, dysarthria (speech
disturbance)

42. 42
42
Contraindications:
Contraindications:




Hypotension
Hypotension
Ischemic heart disease
Ischemic heart disease
Glaucoma
Glaucoma
Liver and kidney function disorders
Liver and kidney function disorders

43. 43
43
First aid in overdosage with ganglion
blockers
First aid in overdosage with ganglion
blockers
First aid in overdosage with ganglion
blockers



Introduction of pharmacological antagonists
(anticholinesterases), analeptics
Introduction of pharmacological antagonists
(anticholinesterases), analeptics
Introduction of pharmacological antagonists
(anticholinesterases), analeptics
Artificial lung ventilation (ALV)
Artificial lung ventilation (ALV)
Orthostatic hypotension is releaved by
introduction of vasoconstrictive agents
(Norepinephrine, Phenylephrine)
Orthostatic hypotension is releaved by
introduction of vasoconstrictive agents
(Norepinephrine, Phenylephrine)
Orthostatic hypotension is releaved by
introduction of vasoconstrictive agents
(Norepinephrine, Phenylephrine)
Orthostatic hypotension is releaved by
introduction of vasoconstrictive agents
(Norepinephrine, Phenylephrine)

44. 44
44
Skeletal muscle relaxants
(neuromuscular blockers)
Skeletal muscle relaxants
(neuromuscular blockers)
Skeletal muscle relaxants
(neuromuscular blockers)
 Skeletal muscle relaxants (curare-like
agents) cause total relaxation of skeletal
muscles due to selective block of
Skeletal muscle relaxants (curare-like
agents) cause total relaxation of skeletal
muscles due to selective block of
Skeletal muscle relaxants (curare-like
agents) cause total relaxation of skeletal
muscles due to selective block of
Skeletal muscle relaxants (curare-like
agents) cause total relaxation of skeletal
muscles due to selective block of
Skeletal muscle relaxants (curare-like
agents) cause total relaxation of skeletal
muscles due to selective block of
Skeletal muscle relaxants (curare-like
agents) cause total relaxation of skeletal
muscles due to selective block of
Skeletal muscle relaxants (curare-like
agents) cause total relaxation of skeletal
muscles due to selective block of
Nm-cholinoceptors and stoppage of
neuro-muscular transmission in neuro-
muscular synapses – myoparalytic effect
(paralysis of skeletal muscles)
Nm-cholinoceptors and stoppage of
neuro-muscular transmission in neuro-
muscular synapses – myoparalytic effect
(paralysis of skeletal muscles)
Nm-cholinoceptors and stoppage of
neuro-muscular transmission in neuro-
muscular synapses – myoparalytic effect
(paralysis of skeletal muscles)
Nm-cholinoceptors and stoppage of
neuro-muscular transmission in neuro-
muscular synapses – myoparalytic effect
(paralysis of skeletal muscles)
Nm-cholinoceptors and stoppage of
neuro-muscular transmission in neuro-
muscular synapses – myoparalytic effect
(paralysis of skeletal muscles)
Nm-cholinoceptors and stoppage of
neuro-muscular transmission in neuro-
muscular synapses – myoparalytic effect
(paralysis of skeletal muscles)

45. 45
45
Pharmacodynamics of muscle relaxants
Pharmacodynamics of muscle relaxants




Non-depolarizing (antidepolarizing) muscle
relaxants
Non-depolarizing (antidepolarizing) muscle
relaxants
Non-depolarizing (antidepolarizing) muscle
relaxants
Most of them act as competitive antagonists of
Асh
Most of them act as competitive antagonists of
Асh
Most of them act as competitive antagonists of
Асh
They block Nm-cholinoceptors of postsynaptic
membrane of neuromuscular synapse and prevent
depolarizing action of Ach
They block Nm-cholinoceptors of postsynaptic
membrane of neuromuscular synapse and prevent
depolarizing action of Ach
They block Nm-cholinoceptors of postsynaptic
membrane of neuromuscular synapse and prevent
depolarizing action of Ach
They block Nm-cholinoceptors of postsynaptic
membrane of neuromuscular synapse and prevent
depolarizing action of Ach
Postsynaptic membrane at that stays non-
depolarized
Postsynaptic membrane at that stays non-
depolarized
Postsynaptic membrane at that stays non-
depolarized
Transmission of impulses from nerve endings to
skeletal muscles is blocked, as a result, skeletal
muscles are relaxed.
Transmission of impulses from nerve endings to
skeletal muscles is blocked, as a result, skeletal
muscles are relaxed.
Transmission of impulses from nerve endings to
skeletal muscles is blocked, as a result, skeletal
muscles are relaxed.
Transmission of impulses from nerve endings to
skeletal muscles is blocked, as a result, skeletal
muscles are relaxed.

46. 46
46
Depolarizing muscle relaxants
Depolarizing muscle relaxants




Suxamethonium chloride -
Suxamethonium chloride -
Suxamethonium chloride -
(doubled molecule of acetylcholine)
(doubled molecule of acetylcholine)
(doubled molecule of acetylcholine)
(doubled molecule of acetylcholine)
interacts with Nm-cholinoreceptors of
postsynaptic membrane, causes its stable
depolarization
interacts with Nm-cholinoreceptors of
postsynaptic membrane, causes its stable
depolarization
interacts with Nm-cholinoreceptors of
postsynaptic membrane, causes its stable
depolarization
interacts with Nm-cholinoreceptors of
postsynaptic membrane, causes its stable
depolarization
desensitization (loss of sensitivity) of
receptors and neuromuscular block occur
desensitization (loss of sensitivity) of
receptors and neuromuscular block occur
desensitization (loss of sensitivity) of
receptors and neuromuscular block occur
A muscle contracts, then relaxes
A muscle contracts, then relaxes
Microtrauma of fibers and muscle pains are
observed in postoperative period
Microtrauma of fibers and muscle pains are
observed in postoperative period
Microtrauma of fibers and muscle pains are
observed in postoperative period

47. 47
47
Depolarizing muscle relaxants
Depolarizing muscle relaxants




Anticholineasterases potentiate (enhance)
action of depolarizing muscle relaxats
Anticholineasterases potentiate (enhance)
action of depolarizing muscle relaxats
Anticholineasterases potentiate (enhance)
action of depolarizing muscle relaxats
Inactivation of depolarizing muscle relaxants is
realized by pseudocholinesterase –
butyrylcholinesterase of plood plasma
Inactivation of depolarizing muscle relaxants is
realized by pseudocholinesterase –
butyrylcholinesterase of plood plasma
Inactivation of depolarizing muscle relaxants is
realized by pseudocholinesterase –
butyrylcholinesterase of plood plasma
Inactivation of depolarizing muscle relaxants is
realized by pseudocholinesterase –
butyrylcholinesterase of plood plasma
Inactivation of depolarizing muscle relaxants is
realized by pseudocholinesterase –
butyrylcholinesterase of plood plasma
Inactivation of depolarizing muscle relaxants is
realized by pseudocholinesterase –
butyrylcholinesterase of plood plasma
In overdosage of DMR transfusion of fresh donor
blood can be recommended, but not
anticholinestarase agents
In overdosage of DMR transfusion of fresh donor
blood can be recommended, but not
anticholinestarase agents
In overdosage of DMR transfusion of fresh donor
blood can be recommended, but not
anticholinestarase agents
In overdosage of DMR transfusion of fresh donor
blood can be recommended, but not
anticholinestarase agents
practically: Artificial lung ventilation (ALV) is
performed, in 5-10‘ the drug is destroyed
practically: Artificial lung ventilation (ALV) is
performed, in 5-10‘ the drug is destroyed
practically: Artificial lung ventilation (ALV) is
performed, in 5-10‘ the drug is destroyed
practically: Artificial lung ventilation (ALV) is
performed, in 5-10‘ the drug is destroyed

48. 48
48
Muscle relaxants of mixed action
Muscle relaxants of mixed action
 Dioxonium - is seldom used
Dioxonium - is seldom used
Dioxonium - is seldom used
Dioxonium - is seldom used
initially it acts like depolarizing muscle
relaxants (cause depolarization of
membrane), then membrane potential is
restored, but receptors are blocked for
action of acetylcholine similar to
antidepolarizing muscle relaxants)
initially it acts like depolarizing muscle
relaxants (cause depolarization of
membrane), then membrane potential is
restored, but receptors are blocked for
action of acetylcholine similar to
antidepolarizing muscle relaxants)
initially it acts like depolarizing muscle
relaxants (cause depolarization of
membrane), then membrane potential is
restored, but receptors are blocked for
action of acetylcholine similar to
antidepolarizing muscle relaxants)
initially it acts like depolarizing muscle
relaxants (cause depolarization of
membrane), then membrane potential is
restored, but receptors are blocked for
action of acetylcholine similar to
antidepolarizing muscle relaxants)
initially it acts like depolarizing muscle
relaxants (cause depolarization of
membrane), then membrane potential is
restored, but receptors are blocked for
action of acetylcholine similar to
antidepolarizing muscle relaxants)
initially it acts like depolarizing muscle
relaxants (cause depolarization of
membrane), then membrane potential is
restored, but receptors are blocked for
action of acetylcholine similar to
antidepolarizing muscle relaxants)
initially it acts like depolarizing muscle
relaxants (cause depolarization of
membrane), then membrane potential is
restored, but receptors are blocked for
action of acetylcholine similar to
antidepolarizing muscle relaxants)

49. 49
49
Administration of muscle relaxants
Administration of muscle relaxants



Anesthesiology and surgery:
Anesthesiology and surgery:
they used for relaxation of skeletal
muscles in reduction of dislocations,
reposition of bone (fractured) fragments,
intubation of trachea, endoscopy,
laryngospasm, assisted ventillation (ALV)
they used for relaxation of skeletal
muscles in reduction of dislocations,
reposition of bone (fractured) fragments,
intubation of trachea, endoscopy,
laryngospasm, assisted ventillation (ALV)
they used for relaxation of skeletal
muscles in reduction of dislocations,
reposition of bone (fractured) fragments,
intubation of trachea, endoscopy,
laryngospasm, assisted ventillation (ALV)
they used for relaxation of skeletal
muscles in reduction of dislocations,
reposition of bone (fractured) fragments,
intubation of trachea, endoscopy,
laryngospasm, assisted ventillation (ALV)
they used for relaxation of skeletal
muscles in reduction of dislocations,
reposition of bone (fractured) fragments,
intubation of trachea, endoscopy,
laryngospasm, assisted ventillation (ALV)
they used for relaxation of skeletal
muscles in reduction of dislocations,
reposition of bone (fractured) fragments,
intubation of trachea, endoscopy,
laryngospasm, assisted ventillation (ALV)
they used for relaxation of skeletal
muscles in reduction of dislocations,
reposition of bone (fractured) fragments,
intubation of trachea, endoscopy,
laryngospasm, assisted ventillation (ALV)
they used for relaxation of skeletal
muscles in reduction of dislocations,
reposition of bone (fractured) fragments,
intubation of trachea, endoscopy,
laryngospasm, assisted ventillation (ALV)
they used for relaxation of skeletal
muscles in reduction of dislocations,
reposition of bone (fractured) fragments,
intubation of trachea, endoscopy,
laryngospasm, assisted ventillation (ALV)
they used for relaxation of skeletal
muscles in reduction of dislocations,
reposition of bone (fractured) fragments,
intubation of trachea, endoscopy,
laryngospasm, assisted ventillation (ALV)
Convusions, severe cases of tetanus and
status epilepticus
Convusions, severe cases of tetanus and
status epilepticus
Convusions, severe cases of tetanus and
status epilepticus
Muscles are relaxed in certain order: muscles of
face and neck, extremities and trunk, respiratory
muscles and diaphragm
Muscles are relaxed in certain order: muscles of
face and neck, extremities and trunk, respiratory
muscles and diaphragm
Muscles are relaxed in certain order: muscles of
face and neck, extremities and trunk, respiratory
muscles and diaphragm
Muscles are relaxed in certain order: muscles of
face and neck, extremities and trunk, respiratory
muscles and diaphragm
Muscles are relaxed in certain order: muscles of
face and neck, extremities and trunk, respiratory
muscles and diaphragm
Muscles are relaxed in certain order: muscles of
face and neck, extremities and trunk, respiratory
muscles and diaphragm
Muscle relaxants are used when ALV apparatus is
available.
Muscle relaxants are used when ALV apparatus is
available.
Muscle relaxants are used when ALV apparatus is
available.
Muscle relaxants are used when ALV apparatus is
available.

50. 50
50
Administration of muscle relaxants
Administration of muscle relaxants


They are quaternary ammonium
compounds, and so they badly absorbed
from GIT and used only intravenously
They are quaternary ammonium
compounds, and so they badly absorbed
from GIT and used only intravenously
They are quaternary ammonium
compounds, and so they badly absorbed
from GIT and used only intravenously
They are quaternary ammonium
compounds, and so they badly absorbed
from GIT and used only intravenously
A drug Mellictinum is tertiary base, it is a
single muscle relaxant in the form of
tablets.
A drug Mellictinum is tertiary base, it is a
single muscle relaxant in the form of
tablets.
A drug Mellictinum is tertiary base, it is a
single muscle relaxant in the form of
tablets.
A drug Mellictinum is tertiary base, it is a
single muscle relaxant in the form of
tablets.
A drug Mellictinum is tertiary base, it is a
single muscle relaxant in the form of
tablets.
A drug Mellictinum is tertiary base, it is a
single muscle relaxant in the form of
tablets.
It decreases tone of skeletal muscles not
producing their paralysis
It decreases tone of skeletal muscles not
producing their paralysis
It decreases tone of skeletal muscles not
producing their paralysis

51. 51
51
Adverse effects of muscle relaxants
Adverse effects of muscle relaxants


Depolarizing ones:
Depolarizing ones:
cardiac arrhythmia, ABP rise
cardiac arrhythmia, ABP rise
cardiac arrhythmia, ABP rise
Muscle pains in postoperative period
Muscle pains in postoperative period
↑ intraocular tension and intracranial
pressure, myoglobinemia, hyperkaliemia
↑ intraocular tension and intracranial
pressure, myoglobinemia, hyperkaliemia
↑ intraocular tension and intracranial
pressure, myoglobinemia, hyperkaliemia
↑ intraocular tension and intracranial
pressure, myoglobinemia, hyperkaliemia
↑ intraocular tension and intracranial
pressure, myoglobinemia, hyperkaliemia
↑ intraocular tension and intracranial
pressure, myoglobinemia, hyperkaliemia
↑ intraocular tension and intracranial
pressure, myoglobinemia, hyperkaliemia
Antidepolarizing ones:
Antidepolarizing ones:
Antidepolarizing ones:
arterial hypotension,
arterial hypotension,
bradycardia or tachycardia,
bradycardia or tachycardia,
myocardium ischemia,
myocardium ischemia,
ventricular extrasystoles,
ventricular extrasystoles,
bronchospasm
bronchospasm

52. Antagonists of muscle relaxants
Antagonists of muscle relaxants


Neostigmine 0.5-2.0mg i.v., preceded by
Atropine to block muscarinic effects,
rapidly reverses paralysis induced by
competitive neuromuscular blockers
Neostigmine 0.5-2.0mg i.v., preceded by
Atropine to block muscarinic effects,
rapidly reverses paralysis induced by
competitive neuromuscular blockers
Neostigmine 0.5-2.0mg i.v., preceded by
Atropine to block muscarinic effects,
rapidly reverses paralysis induced by
competitive neuromuscular blockers
Neostigmine 0.5-2.0mg i.v., preceded by
Atropine to block muscarinic effects,
rapidly reverses paralysis induced by
competitive neuromuscular blockers
Neostigmine 0.5-2.0mg i.v., preceded by
Atropine to block muscarinic effects,
rapidly reverses paralysis induced by
competitive neuromuscular blockers
Neostigmine 0.5-2.0mg i.v., preceded by
Atropine to block muscarinic effects,
rapidly reverses paralysis induced by
competitive neuromuscular blockers
Sugammadex is new antagonist of
antidepolarazing muscle relaxants. Its
use does not need Atropine.
Sugammadex is new antagonist of
antidepolarazing muscle relaxants. Its
use does not need Atropine.
Sugammadex is new antagonist of
antidepolarazing muscle relaxants. Its
use does not need Atropine.
Sugammadex is new antagonist of
antidepolarazing muscle relaxants. Its
use does not need Atropine.
Sugammadex is new antagonist of
antidepolarazing muscle relaxants. Its
use does not need Atropine.
52
52