Hello friends. In this PPT I am talking about autonomic nervous system. If you like it, please do let me know in the comments section. A single word of appreciation from you will encourage me to make more of such videos. Thanks. Enjoy and welcome to the beautiful world of pharmacology where pharmacology comes to life. This video is intended for MBBS, BDS, paramedical and any person who wishes to have a basic understanding of the subject in the simplest way.
2. Noradrenergic transmission
• Restricted to the sympathetic division of the ANS
1. Norepinephrine Postganglionic sympathetic
neurons sites (except at sweat glands, hair
follicles and some vasodilator fibres) and in
certain areas of brain.
2. Epinephrine Adrenal medulla
3. Dopamine Renal and mesenteric vasculature
16. • When a drug or a physiologic action increases
blood pressure, this activates stretch receptors
(mechanoreceptors) located in the aortic arch and
in the carotid sinus at the bifurcation of the carotid
artery
• Receptor activation initiates impulses that travel via
afferent nerves to the brain stem vasomotor center
• Stimulation of the vagal motor nucleus (via nerves
from the solitary tract nucleus) leads to an increase
in vagal (parasympathetic) outflow, a decrease in
heart rate, and a decrease in the sympathetic nerve
outflow from the vasomotor center
• The effect on the heart rate is called reflex
bradycardia
19. • Phenoxybenzamine is an irreversible antagonist
whereas Phentolamine and Tolazoline are
reversible blockers of α1 and α2 receptors
Vasodilation and postural hypotension
• Reflex increase in sympathetic discharge and
increased sympathetic outflow (due to blockade of
α2 receptors) are responsible for marked
tachycardia seen with the use of these agents
20. • Use of these drugs before adrenaline results in
vasomotor reversal of Dale
• Intravenous injection of adrenaline normally causes
increase in blood pressure (α effect) followed by
prolonged fall (β2 effect)
• If it is administered after giving α blockers, only fall
in BP is seen (vasomotor reversal of Dale)
22. Administration
• CAs are absorbed from the intestine but are rapidly
degraded by MAO & COMT present in the intestinal
wall and liver (orally inactive)
• Adrenaline (epinephrine) is administered by s.c. or
i.m. injection in a dose of 0.2–0.5 mg; action lasts
0.5–2 hours.
• In dental practice, it is used as a local vasoconstr.
added to lidocaine in a concentration of 1 in
200,000 to 80,000 for dental anaesthesia.
23. Dopamine
• Low doses (< 2 μg/kg per min) D1 dopaminergic
receptors in renal, mesenteric, and coronary
vascular beds (vasodilation); activates adenylyl
cyclase in vascular smooth muscle cells, leading to
↑ cAMP levels and vasodilation
• Moderate dose (2–10 μg/kg per min) β1 recept.
(positive inotrope)
• Higher dose (>10 μg/kg per min) α1 receptors
(vasoconstriction)
24. Adrenaline
Uses (ABCDE)
1. Anaphylactic shock (DOC) 0.5 mg (0.5 ml of 1
in 1000 solution for adult) i.m.
2. Bronchial asthma
3. Cardiac arrest 10 ml of 1:10000 i.v.
4. Control of local bleeding Adr 1 in 10,000
5. During LA combined with Lignocaine (1:50,000 or
1:2,00,000)
6. To control Epistaxis
26. • The LA often fails to afford adequate pain control in
inflamed tissues (like infected tooth)
• The likely reasons are:
1. Inflammation lowers pH of the tissue— greater
fraction of the LA is in the ionized form hindering
diffusion into the axolemma
2. Blood flow to the inflamed area is increased—the
LA is removed more rapidly from the site
3. Effectiveness of Adr injected with the LA is
reduced at the inflamed site
4. Inflammatory products may oppose LA action
27. • Addition of a vasoconstrictor, e.g. adrenaline
(1:50,000 to 1:200,000):
1. Prolongs duration of action of LAs by decreasing
their rate of removal from the local site into the
circulation
2. Enhances the intensity of nerve block
3. Reduces systemic toxicity of LAs: rate of
absorption is reduced and metabolism keeps the
plasma concentration lower
28. 4. Provides a more bloodless field for surgery
5. Increases the chances of subsequent local tissue
edema and necrosis as well as delays wound healing
by reducing oxygen supply and enhancing oxygen
consumption in the affected area
6. May raise BP and promote arrhythmia in
susceptible individuals
29. Adverse Effects
1. Transient restlessness, headache, palpitation,
anxiety, tremor and pallor may occur after s.c./
i.m. injection of Adr
2. Marked rise in BP leading to cerebral
haemorrhage, ventricular tachycardia/fibrillation,
angina, myocardial infarction are the hazards of
large doses or inadvertant i.v. injection of Adr
30. Contraindications
1. Adr is contraindicated in hypertensive,
hyperthyroid and angina patients
2. Adr should not be given during anaesthesia with
halothane (risk of arrhythmias) and to patients
receiving β blockers (marked rise in BP can occur
due to unopposed α action)
3. Adr mixed local anaesthetic should be used very
cautiously for dental anaesthesia in patients with
heart disease
31. Dobutamine
• Selective β1 rec. agonist
• Prominent action ↑ force of cardiac contraction
and output, without significant change in heart
rate, peripheral resistance and BP
• Uses
1. Pump failure accompanying myocardial infarction
2. Cardiac surgery
3. Short term management of severe congestive
heart failure
32. Phenylephrine
• Selective α1 agonist (↑ BP by causing
vasoconstriction)
• Uses
1. Nasal decongestant
2. Fundus examination (cycloplegia not required)
Notas del editor
Baroreceptors are mechanoreceptors located in the carotid sinus and in the aortic arch. Their function is to sense pressure changes by responding to change in the tension of the arterial wall. The baroreflex mechanism is a fast response to changes in blood pressure.
1, Increased arterial pressure activates stretch receptors in the aortic arch and carotid sinus. 2, Receptor activation initiates afferent impulses to the brainstem vasomotor center (VMC). 3, Via solitary tract fibers, the VMC activates the vagal motor nucleus, which increases vagal (parasympathetic) outflow and slows the heart. At the same time, the VMC reduces stimulation of spinal intermediolateral neurons that activate sympathetic preganglionic fibers, and this decreases sympathetic stimulation of the heart and blood vessels. By this mechanism, drugs that increase blood pressure produce reflex bradycardia. Drugs that reduce blood pressure attenuate this response and cause reflex tachycardia
MAP=DBP + 1/3 PP
CAs are absorbed from the intestine but are rapidly degraded by MAO and COMT present in the intestinal wall and liver. They are thus orally inactive. For systemic effects Adrenaline (epinephrine) is administered by s.c. or i.m. injection in a
dose of 0.2–0.5 mg; action lasts 0.5–2 hours. In dental practice, it is used as a local vasoconstrictor added to lidocaine in a concentration of 1 in 200,000 to 80,000 for dental anaesthesia.
The heart is innervated by vagal and sympathetic fibers. The right vagus nerve primarily innervates the SA node, whereas the left vagus innervates the AV node; however, there can be significant overlap in the anatomical distribution. Atrial muscle is also innervated by vagal efferents, whereas the ventricular myocardium is only sparsely innervated by vagal efferents. Sympathetic efferent nerves are present throughout the atria (especially in the SA node) and ventricles, including the conduction system of the heart.
Sympathetic stimulation of the heart increases heart rate (positive chronotropy), inotropy and conduction velocity (positive dromotropy), whereas parasympathetic stimulation of the heart has opposite effects. Sympathetic and parasympathetic effects on heart function are mediated by beta-adrenoceptors and muscarinic receptors, respectively.