Autonomic Pharmacology (Ar) - Lec 01 Part 1 - Review of physiology
Summary
TLDRThis video provides a concise review of the principles of physiology of the autonomic nervous system (ANS), essential for understanding pharmacology. The ANS regulates involuntary functions and consists of the sympathetic and parasympathetic systems. The video covers the roles of higher centers, nerves, chemical transmitters, and receptors in both systems. It explains how autonomic nerves transmit signals, the significance of ganglia, the fate of neurotransmitters like acetylcholine, and the impact of various receptors on internal organs. The importance of drug selectivity and the implications of enzyme deficiencies are also discussed to aid in comprehending autonomic malfunction treatments.
Takeaways
- 😀 The autonomic nervous system (ANS) regulates involuntary functions such as those of the intestines, lungs, and heart.
- 😀 The ANS is divided into the sympathetic and parasympathetic systems, each with higher centers, nerves, chemical transmitters, and receptors.
- 😀 Higher centers in the brain and spinal cord control autonomic functions, sending signals via nerves to internal organs.
- 😀 Autonomic nerves rely on ganglia, which act as relay stations; sympathetic ganglia are near the spinal cord, while parasympathetic ganglia are near organs.
- 😀 Most internal organs have dual nerve supply from both sympathetic and parasympathetic systems, but the ratio of nerve supply can vary.
- 😀 Nerve signals in the ANS are transmitted by chemical neurotransmitters; acetylcholine is released in both systems at ganglia, while norepinephrine is released at sympathetic nerve endings.
- 😀 Receptors for neurotransmitters include nicotinic acetylcholine receptors in ganglia and muscarinic or adrenergic receptors at nerve terminals on organs.
- 😀 Drugs can target different levels of the ANS: higher centers, ganglia, nerve endings, and receptors, with receptor-level targeting being the most selective.
- 😀 Acetylcholine is broken down by cholinesterase enzymes; true cholinesterase is specific to acetylcholine, while pseudocholinesterase (butyrylcholinesterase) breaks down multiple substances.
- 😀 Deficiencies in pseudocholinesterase can lead to severe reactions to drugs like succinylcholine, used as a muscle relaxant during surgeries, resulting in prolonged muscle paralysis.
Q & A
What is the primary focus of the video series on pharmacology?
-The primary focus of the video series is a quick revision on the principles of physiology of the autonomic nervous system, which is necessary for understanding the mechanism of action of drugs in this chapter.
What are the two divisions of the autonomic nervous system?
-The two divisions of the autonomic nervous system are the sympathetic and parasympathetic systems.
What are the four elements discussed in relation to each system in the autonomic nervous system?
-The four elements discussed are higher centers, nerves, chemical transmitters, and receptors.
What role do higher centers play in the autonomic nervous system?
-Higher centers control all autonomic or visceral functions of the body and can be targeted by drugs to control the autonomic nervous system.
How do autonomic nerves differ from motor nerves in terms of their travel distance?
-Autonomic nerves do not travel the whole distance as one segment. They first rely on a station called a ganglion, which regulates the strength of signals before reaching internal organs.
What is the main difference between the ganglia of the parasympathetic and sympathetic systems?
-Parasympathetic ganglia are situated near the organs, while sympathetic ganglia are found very far from the organs and close to the spinal cord.
What neurotransmitter is released in both parasympathetic and sympathetic ganglia?
-Acetylcholine is the neurotransmitter released in both parasympathetic and sympathetic ganglia.
What type of receptors does acetylcholine act on in ganglia?
-Acetylcholine acts on nicotinic acetylcholine receptors in ganglia.
What are the main adrenergic receptors in the sympathetic system?
-The main adrenergic receptors in the sympathetic system are alpha-1, alpha-2, beta-1, beta-2, and beta-3 receptors.
Why are ganglion blockers no longer used in controlling the autonomic nervous system?
-Ganglion blockers are no longer used because they are non-selective and affect both sympathetic and parasympathetic ganglia, leading to depression of all autonomic functions throughout the body.
How can we selectively control the autonomic nervous system at the level of receptors?
-We can selectively control the autonomic nervous system at the level of receptors by using drugs that target specific receptor subtypes, such as beta-1 blockers or alpha-1 blockers.
What happens to acetylcholine after it performs its function on the receptor?
-After performing its function on the receptor, acetylcholine must be broken down immediately by choline esterase enzymes to prevent continuous stimulation.
What are the two types of choline esterase enzymes, and what are their roles?
-The two types of choline esterase enzymes are true choline esterase (acetylcholine esterase), which specifically breaks down acetylcholine, and pseudocholine esterase (butyrylcholinesterase), which is non-specific and breaks down various choline esters, including some drugs.
What potential problem can arise in patients with pseudocholine esterase deficiency during surgery?
-Patients with pseudocholine esterase deficiency can experience prolonged muscle paralysis and respiratory inhibition if given succinylcholine, a muscle relaxant, because the enzyme responsible for breaking down the drug is deficient.
Outlines
🧠 Introduction to the Autonomic Nervous System
This video introduces the principles of the autonomic nervous system (ANS) essential for understanding drug mechanisms in pharmacology. The ANS regulates visceral functions such as those of the heart and intestines, operating subconsciously. The ANS comprises the sympathetic and parasympathetic systems, each with four key elements: higher centers, nerves, chemical transmitters, and receptors. The video focuses on higher centers, nerves, and chemical transmitters, illustrating the brain, spinal cord, and control centers for autonomic functions.
❤️ Dual Nerve Supply to Organs
The heart is used as an example to explain the dual nerve supply from the sympathetic and parasympathetic systems. Most internal organs receive dual nerve supplies, although not always equally. Nerve signals from higher centers pass through the spinal cord to reach organs via nerve terminals. The video discusses ganglia as relay stations for autonomic nerves, situated near organs for the parasympathetic system and close to the spinal cord for the sympathetic system. These differences can be important in clinical scenarios.
⚡ Mechanisms of Neurotransmitter Release
The process of neurotransmission in the autonomic nervous system is described, highlighting how acetylcholine is released at ganglia and nerve terminals to activate receptors. The sympathetic system primarily releases norepinephrine, while the parasympathetic system releases acetylcholine at nerve endings. Receptor types are specified: muscarinic receptors (M1, M2, M3) for parasympathetic actions and adrenergic receptors (alpha-1, alpha-2, beta-1, beta-2, beta-3) for sympathetic actions. Each organ predominantly expresses certain receptor subtypes.
⚖️ Treating Autonomic Dysfunction
The video explains how to treat autonomic dysfunctions like tachycardia and bradycardia by targeting specific receptors. For example, beta-blockers can manage overactive sympathetic responses causing tachycardia, while drugs affecting M2 receptors can address bradycardia. This section summarizes the control of the autonomic nervous system at higher centers, ganglia, nerve endings, and receptors, with a preference for targeting receptors due to their selectivity.
🔬 Fate of Neurotransmitters
This section discusses the breakdown of neurotransmitters like acetylcholine by enzymes after their release and action. Two types of cholinesterase enzymes are described: true acetylcholinesterase, which specifically breaks down acetylcholine, and pseudocholinesterase, which also breaks down other substances like succinylcholine. The video highlights the significance of these enzymes in maintaining neurotransmitter balance and the implications of their inhibition or genetic deficiencies.
💉 Clinical Implications of Enzyme Deficiencies
The importance of cholinesterase enzymes is illustrated through the example of succinylcholine metabolism. A genetic deficiency in pseudocholinesterase can lead to prolonged muscle paralysis and respiratory issues during surgery. The video explains how anesthesiologists account for this enzyme's activity when dosing succinylcholine. This section emphasizes understanding enzyme functions and genetic variability for safe pharmacological interventions.
Mindmap
Keywords
💡Autonomic Nervous System
💡Sympathetic Nervous System
💡Parasympathetic Nervous System
💡Higher Centers
💡Ganglia
💡Acetylcholine
💡Nicotinic Acetylcholine Receptor
💡Norepinephrine
💡Adrenergic Receptors
💡Cholinesterase Enzyme
Highlights
The autonomic nervous system (ANS) regulates all visceral functions without conscious control, including those of the intestines, lungs, and heart.
The ANS is divided into two systems: the sympathetic and the parasympathetic systems, each controlling different aspects of bodily functions.
Higher centers control autonomic functions through the brain, spinal cord, and nerve networks, which then regulate internal organs.
Sympathetic nerves (depicted in red) and parasympathetic nerves (depicted in black) originate from higher centers and control organ functions.
Most internal organs have a dual nerve supply from both sympathetic and parasympathetic systems, providing a balanced control mechanism.
Autonomic nerves rely on ganglia, which act as power stations to regulate signal strength before reaching internal organs.
Parasympathetic ganglia are located near organs, while sympathetic ganglia are situated close to the spinal cord, known as paravertebral ganglia.
Acetylcholine is a key neurotransmitter in the ANS, released at nerve terminals to activate receptors.
Parasympathetic nerve endings release acetylcholine, which acts on muscarinic receptors (M1, M2, M3) to regulate organ functions.
Sympathetic nerve endings release norepinephrine (noradrenaline), which acts on adrenergic receptors (alpha-1, alpha-2, beta-1, beta-2, beta-3).
Organs do not have all receptor types; instead, specific receptor subtypes predominate, such as M2 receptors in the heart for parasympathetic control.
The antagonistic function of sympathetic and parasympathetic systems ensures balanced control of organ functions, such as heart rate.
Autonomic dysfunctions, like tachycardia or bradycardia, can be treated by targeting specific receptors with drugs.
Drugs can control the ANS at higher centers, nerve endings, or receptors, with receptor-level control being the most selective and effective.
Acetylcholine must be rapidly broken down by enzymes (acetylcholinesterase or butyrylcholinesterase) after performing its function to prevent prolonged activation.
Butyrylcholinesterase, produced by the liver, is a non-specific enzyme that metabolizes various substances, including some drugs used in anesthesia.
Deficiency in butyrylcholinesterase can lead to prolonged effects of certain drugs, causing conditions like succinylcholine apnea during surgery.
Transcripts
hello everyone welcome to pharmacology
illustration series
we will specify this video and the next
one for a quick revision on principles
of physiology of the autonomic nervous
system
this is the background we need to be
able to understand the mechanism of
action of all drugs in this chapter
of course we don't need to explain all
principles of physiology however certain
points must be clarified to be able to
comprehend principles of pharmacology in
this chapter
first of all you should know that
autonomic nervous system is the division
of nervous system concerned with
regulation of autonomic function which
means all of visceral functions we have
as those of intestine lung heart or
whatever are not controlled of the
conscious level but are under control of
the autonomic nervous system which has
two divisions the sympathetic and the
parasympathetic systems and in each
system we need to discuss four elements
which are higher centers
nerves
chemical transmitters
and receptors
in this video we will explain the higher
centers nerves and chemical transmitters
seven receptors for discussion on the
next video now let's concentrate on this
drawing here
this is the brain the spinal cord and
here we have the higher centers
we will cover the sympathetic system
with red and the parasympathetic system
with black
these are the higher centers that
control all autonomic or visceral
function of the whole body when we say
higher centers we are talking about them
collectively to be more specific we have
centers here Omid Allah and centers
above and the hypothalamus above which
are centers in the articular information
and then we have centers in the cortex
centers in these levels are called
higher centers and now we can control
the autonomic function by drugs that act
on these centers
in this chapter we will have many drugs
which control the autonomic nervous
system by acting on these centers these
higher centers will send nerves passing
through spinal cord redkara is for
sympathetic nerves while black one has
four parasympathetic nerves
this autonomic nerve Supply will reach
any organ
so let's take the heart as an example of
the involuntary control of the autonomic
nervous system on such organs here you
see a dual nerve Supply composed of
sympathetic and parasympathetic nerve
fibers
and many but not all internal organs
have dual nerve supply of sympathetic
system and parasympathetic system nerve
fibers
to summarize
nerves is coming from higher centers
passing through the spinal cord until it
reach the internal organ and end with
what is known as nerve terminal and
those nerve terminals of sympathetic
system are different from those of the
parasympathetic system before discussing
how they are different from one another
you should know that autonomic nerves
don't travel the whole distance as one
segment like motor nerves do however
autonomic nerves must firstly rely on a
station
called ganglion which is composed of
collection of neurons
this ganglia act as a power station
regulating the strength of signals
before reaching the internal organs any
autonomic nerve must relay on ganglia
and in case of parasympathetic system
ganglia are situated near the organs but
in case of sympathetic system ganglia
are found very far from organs and close
to the spinal cord that's why it's
called
paravertebral gangly and this difference
is a rich source for questions an
examiner may put you through the
following scenario imagine if you were
in a lab and then we isolated a rabbit
heart and gave it to you and told you to
apply a certain medication on it now
tell me how can the drug affect the
isolated organ your answer as a student
will be like thus
the drug can act upon nerve terminals
either sympathetic or parasympathetic
and it can also act on a receptor and
that is reasonable because the Earth
terminals act by releasing transmitters
that activate receptors so the drug can
indeed act in a receptor
but if you say the drug can act on
ganglia here the examiner would ask you
to be more specific
and if you say sympathetic ganglia then
you have fallen into the examiner's
track when we isolate an organ it comes
with its parasympathetic ganglia only as
it is always situated close to the organ
side so when a drug is applied to an
isolated organ
it can act on a receptor nerve terminals
or parasympathetic ganglia specifically
now you may wonder if all internal
organs have dual Supply both systems the
answer is most but not all have dual
Supply however nerve supply of both
systems to an organ is rarely equal
sometimes the ratio of nerve Supply is
50 50 sometimes one system is given 80
percent of the autonomic nerves applied
to an organ while the other is only
contributing by 20 percent down to some
organ which have single supply of only
one system for example single
sympathetic nerve Supply is found in
superiorenal glands which is considered
as modified sympathetic ganglia sweat
gland also have only sympathetic nerve
Supply and most importantly the blood
vessels which are mostly supplied only
by sympathetic nervous system now you
know that most organs have dual nerve
Supply except accepting some organs
which have single Supply as mentioned
before
here we have talked about higher centers
which send fibers through spinal cord
given rise to nerves that Supply our
internal organs
and most of them have dual nerve Supply
but some has single Supply as those
mentioned before
now we need to look at the signal which
is generated in the higher centers then
it passes through the nerve till it
reached the ganglia where the signal in
the form of electrical depolarization
causes release of chemical transmitter
called acetylcholine
in this state
acetylcholine is termed neurotransmitter
then acetylcholine opens a gate inside
the ganglia this gate is considered as
receptor termed nicotinic acetylcholine
receptor
this type of receptor is Ion channel
receptor that will be discussed in the
next chapter of General pharmacology
you will know that this type of receptor
is the fastest one that can respond to
acetylcholine among all other types of
receptors
so now after the style cooling is
released inside the ganglia it opens a
gate named nicotinic acetylcholine
receptor causing sodium ion influx
causing depolarization that's because
during nerve transmission we need a fast
responding receptor type which has
nicotenica style choline receptor which
will generate another signal in the
post-ganglionic fibers in the form of
depolarization wave till it reach the
nerve endings again signals coming from
higher centers as depolarization wave
pulsing through nerves to reaching the
ganglia where it transforms from
electrical into chemical form
so the polarization wave releases
acetylcholine
acetylcholine opens a gate termed
nicotinic acetylcholine receptor when
this gate opens post ganglionic membrane
becomes depolarized and signals come in
this direction
so when pulsed ganglionic fibers are
depolarized the polarization wave
reaches nerve terminals then same
scenario will happen again as this
vesicles filled with acetylcholine where
rupture causing release of acetylcholine
which acts on its receptors present on
this organ now termed cholinergic
receptors and what are these cholinergic
receptors that are found in many organs
called it's called muscarinic receptors
and we have three well-known types of
muscarinic receptors termed in one M2
and M3 m is short for muscarinic and the
number is for the subtype so we have M1
M2 M3 and we also have M4 and M5 but
those two are of little significance
these are the mascarenic receptors which
will be discussed in detail but not
right now this whole system is called
parasympathetic system but what happens
in the sympathetic system
it is nearly the same as parasympathetic
system
higher centers send signals however
pre-ganglionic fibers and sympathetic
system are short as ganglia or situated
close to the spinal cord yet same
process occurs again as depolarization
wave reaches ganglia causing the release
of chemical transmitter which is also
the acetylcholine then acetylcholine
opens a gate called nicotinic
acetylcholine receptor
and when the gate opens it causes sodium
ion influx causing the polarization in
the post-synaptic membrane
then signal continue as depolarization
wave till it reach sympathetic nerve
endings however this time nerve endings
doesn't release
acetylcholine and instead it release
another transmitter termed
norepinephrine or noradrenaline and Tiny
amount of fibers release epinephrine but
most of them release norepinephrine
when vesicles rupture and release nor
adrenaline nor adrenaline acts on a
receptor so what do we call this
receptor
do we call it mascarenic cholinergic no
this time receptors are termed
adrenergic receptors
and what are adrenergic receptors we
have
we have five adrenergic receptors termed
alpha-1 Alpha 2 beta1 beta2 beta3
now I ask you do all internal organs
have all of these receptors
or that the heart has M1 M2 M3 alpha-1
Alpha 2 and so on of course not fans
tend to choose one or two receptors at
Max
for example chooses M2 when it
works under parasympathetic rule so that
we call M2 cardiac M2 receptors
that's because the heart doesn't have
much of M1 nor M3 but mainly M2
receptors
and same goes for sympathetic as most of
sympathetic receptors on the heart or of
beta1 subtype which predominates all the
other types others may be present like
alpha 1 Alpha 2 but they are of no
significance
beta1 receptor pre-dominates them all so
that we call it cardiac beta-1 receptor
to summarize all internal organs have
dual supply of sympathetic and
parasympathetic these two release
chemical transmitter that activates
receptors however organs don't have all
types of receptors and instead one of
each type predominates the other and
they always have antagonistic function
so if one is increasing the function
then the other one is decreasing it
now you may ask what is the benefit of
such antagonism this antagonism prevents
the organ from being controlled by only
one force
for example when one is activated
causing tachycardia the other one can
antagonize it and causes bradycardia but
where does the problem come from
a patient may come to you complaining of
tachycardia or rapid pulse now you
understand that this problem tachycardia
is caused by overactivity of sympathetic
system and this beta receptor is
overactive causing increased heart rate
so how can we treat this patient we can
give him a drug that either blocks this
beta receptor or activates the
antagonistic M2 which is able to
counteract the effect of beta receptor
on the contrary a patient may come to
you complaining of bradycardia so tell
me what's causing this problem yes it's
a parasympathetic system and we can give
him a drug either blocks M2 receptor or
activates beta receptors
so they can reach equilibrium
this background you now have enables you
to understand any autonomic malfunction
and how can you treat it
so can you tell me now what are the
methods of controlling the autonomic
nervous system first of all we can
control the autonomic nervous system at
the level of higher centers secondly we
can control the autonomic nervous system
at the level of ganglia either
sympathetic or parasympathetic ganglia
right we can control it by manipulating
the function of those ganglia
of autonomic nervous system can we
no we can't control the autonomic
nervous system at the level of ganglia
but why can't we control it at the level
of ganglia
it's because you already know that they
have the same chemical composition both
of them either sympathetic or
parasympathetic have the same chemical
transmitter acetylcholine and the same
receptor called nicotinic acetylcholine
receptor so a drug blocks acetylcholine
release is a non-specific drug as it
blocks both sympathetic and
parasympathetic ganglia
which leads to depression of all
autonomic function throughout the body
and this drug lacks a very important
quality which is not being selective
you can't Target acetylcholine or its
nicotenic receptor because in either way
you would be blocking both divisions of
the autonomic nervous system previously
there were drugs known as ganglion
blockers and others called ganglion
stimulants however these drugs are no
longer used due to lack of cell activity
so if an examiner asks you why ganglion
blockers are no longer used you can
simply answer because they are
non-selective and they act on Old
ganglia and thus we can't control their
effects
as such ganglion blockers would cause
depression of all autonomic ganglia
either sympathetic or parasympathetic
and this is a complex effect we do not
desire amidst now back to the original
question can we control autonomic
nervous system on the level of nerve
endings yes we can why because nerve
endings and parasympathetic system
release acetylcholine
button-sympathetic system they release a
different transmitter called nor
epinephrine here we can select one
Division and Target it with a drug acts
either on parasympathetic nerve endings
which release acetylcholine or
sympathetic nerve endings which release
norepinephrine so the second level we
can control autonomic function at as the
level of nerve endings thirdly and this
is the best option which is controlling
it at the level of receptors because
here I can choose even a subtype of
receptor from either divisions in this
chapter we will discuss a group of drugs
called beta-1 blockers that can block
beta1 receptors only orbital one and two
blockers or alpha-1 blockers and so on
and this is the best route being highly
selective so to summarize can we act on
higher centers
yes can we act on ganglia no
can we act on nerve endings yes
can we act on receptors yes and this is
the best route being highly selective
the next step after having understood
the function of nerve endings is the
fate of transmitters transmitters
released from ganglia as acetylcholine
or any other transmitter
we have to understand the fate of
transmitters to decide if it can be of
any value in the signs of pharmacology
now let's focus on this concept after
acetylcholine is released inside ganglia
either by sympathetic or parasympathetic
stimulation and perform a dysfunction on
the receptor
what happens to acetylcholine what is
the feet of acetylcholine you should
know that acetylcholine after performing
its function on the receptor must be
broken down immediately in a matter of
milliseconds
whether this acetylcholine is in the
ganglia or the nerve endings it's broken
down by the action of enzyme called
choline stress enzyme
this is the fate of acetylcholine after
performing its function on the receptor
we have two types of choline stress
enzyme
the fact is true and sudo are pretty old
now true is called
acetylcholine Strays and
pseudoculinistrace is called butyril
choline stress and the differences
between those two enzymes are of utmost
importance now we know that
acetylcholine after performing its
function it must be broken down by
either of two enzymes this through
choline stress is specific which means
it only breaks acetylcholine however
pseudo or butyril enzyme is non-specific
which means it doesn't break down only
acetylcholine but also other chemicals
are destroyed by this pseudo enzyme such
a as her win a well-known drug
it also breaks down procaine and
succinylcholine which will be discussed
later and is used as pre-anesthetic
medication used before surgical
operations as skeletal muscle relaxant
for induction of skeletal muscle
relaxation before surgical operations
this drug is used by anesthesiologists
in certain doses taken into
consideration that it is destroyed by
this enzyme called
sudokoline stress this is about
specificity but what about the site
since it's named true and it is specific
for acetylcholine then you can find it
in all vital areas such as ganglia
CNS and even red blood cells
but why does truecalline Strays present
in red blood cells do we actually have
acetylcholine in our red blood cells
this question will be answered later
however pseudo stress is produced by the
liver and thus you can find it in the
liver and is also present in plasma
again why the pseudoculinous trays
present in plasma do we have circulating
acetylcholine
this is the same question as the first
one however this question will be
answered now
do we have circulating a style choline
in our plasma no we don't have
acetylcholine circulating our bodies so
why do we have pseudoculinous trays in
plasma
the answer is because it is not specific
for acetylcholine so it's present in
plasma to break down many other
compounds such as heroin procaine
succinyl Cooling
even sometimes you may eat food that
contain choline Esters substance similar
to acetylcholine
and Zeus cooling Esters can enter our
blood-causing problems
that's why we need such enzyme in our
plasma and that's why it's sometimes
called biological scavenger
which means it can remove any cooling
Esters weather ingested or injected
now regarding the importance of both
enzymes
if I give you a drug blocks this choline
is Trace enzyme you die because it is
essential for life however this one is
not so much because it is not so
important in breaking down a style
cooling but for metabolism of other
drugs and regarding inhibition of both
enzymes two Strays required three months
to be regenerated again however sudo's
trees only need two weeks to be
regenerated again
okay here we need to lock on the
pseudoculines trace now you know that it
is needed for metabolism of other drugs
than acetyl cooling among these drugs
are succinylcholine a muscle relaxant
drug used before operation to induce
muscle relaxation but do you know some
people have genetic disease with the
gene responsible for pseudoculine stress
synthesis is not present
a child may be born and live his whole
life without knowing that he doesn't
have the gene responsible for cooling
stressed synthesis or the liver
synthesize abnormal form of the enzyme
I have told you this enzyme is not
essential for life
but when does the problem occur
this person can live without any problem
but if he have an operation where
succinylcholine is used the
anesthesiologists consider that 90
percent of this drug is metabolized in
circulation
so he must calculate the dose of
succinyl choline equals 90 percent of
this drug is metabolized before reaching
skeletal muscle so before obtaining the
desired effect on skeletal muscle 90
percent of the drug is eliminated by
pseudoculin stress enzyme so the amount
of drug that escapes the action of the
enzyme and reaches skeletal muscle to
produce its desired effect or only 10
percent of the given do's
now imagine if this child who inherited
a defective Gene from his parents and
didn't know this picture fact
went through an operation where the full
dose of succinyl cooling was
administered those 90 percent of the
Jews won't be metabolized and 100
percent of the those would reach the
muscles
causing not relaxation but muscle
paralysis
and this patient on operation Table
after administering sexy night cooling
to him would start to realize he can't
even breathe
and now he needs a ventilator in order
to survive until the tiny amount of
pseudoculin stress in his plasma can
metabolize and eliminate this drug this
is a fatal case of pseudoculine Strays
enzyme deficiency and because it leads
to respiratory inhibition it is
sometimes called sexy Nile cooling apnea
now I hope you understand the importance
of this background in order to be able
to understand the function of the
autonomic nervous system and how can we
interact with this function
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