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Adrenergic Drugs - drdhriti

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A power point presentation on Adrenergic system and Adrenergic Drugs suitable for Undergraduate MBBS level students

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Adrenergic Drugs - drdhriti

  1. 1. Adrenergic System Dr. D. K. Brahma Department of Pharmacology NEIGRIHMS, Shillong, Meghalaya
  2. 2. Neurotransmission in ANS
  3. 3. Noradrenergic transmission  Nor-adrenaline is the major neurotransmitter of the Sympathetic system  Noradrenergic neurons are postganglionic sympathetic neurons with cell bodies in the sympathetic ganglia  They have long axons which end in varicosities where NA is synthesized and stored
  4. 4. Adrenergic transmission Catecholamines:  Natural: Adrenaline, Noradrenaline, Dopamine  Synthetic: Isoprenaline, Dobutamine Non-Catecholamines:  Ephedrine, Amphetamines, Phenylepherine, Methoxamine, Mephentermine Also called sympathomimetic amines as most of them contain an intact or partially substituted amino (NH2) group
  5. 5. • Catecholamines: Compounds containing a catechol nucleus (Benzene ring with 2 adjacent OH groups) and an amine containing side chain • Non-catecholamines lack hydroxyl (OH) group
  6. 6. Biosynthesis of Catecholamines Phenylalanine PH Rate limiting Enzyme 5-HT, alpha Methyldopa Alpha-methyl-p-tyrosine
  7. 7. Storage of Noradrenaline
  8. 8. Release of NA – Feedback Control
  9. 9. Regulators of NA release
  10. 10. Uptake of Catecholamines
  11. 11. Reuptake  Sympathetic nerves take up amines and release them as neurotransmitters  Uptake I is a high efficiency system more specific for NA  Located in neuronal membrane  Inhibited by Cocaine, TCAD, Amphetamines  Uptake 2 is less specific for NA  Located in smooth muscle/ cardiac muscle  Inhibited by steroids/ phenoxybenzamine  No Physiological or Pharmacological importance
  12. 12. Metabolism of CAs Mono Amine Oxidase (MAO)  Intracellular bound to mitochondrial membrane  Present in NA terminals and liver/ intestine  MAO inhibitors are used as antidepressants  Catechol-o-methyl-transferase (COMT)  Neuronal and non-neuronal tissue  Acts on catecholamines and byproducts  VMA levels are diagnostic for tumours
  13. 13. Metabolism of CAs (Homovanillic acid) (Vanillylmandelic acid)
  14. 14. Adrenergic neurotransmission
  15. 15. Adrenergic Receptors
  16. 16. Adrenergic Receptors  Adrenergic receptors (or adrenoceptors) are a class of G-protein coupled receptors that are the target of catecholamines  Adrenergic receptors specifically bind their endogenous ligands – catecholamines (adrenaline and noradrenline)  Increase or decrease of 2nd messengers cAMP or IP3/DAG  Many cells possess these receptors, and the binding of an agonist will generally cause the cell to respond in a flight-fight manner.  For instance, the heart will start beating quicker and the pupils will dilate
  17. 17. How Many of them ???? Adenoreceptors Alpha (α) Beta (β) α 1 α 2 β1 β 2 β3 α 2A α 2B α 2C α 1A α 1B α 1D
  18. 18. Differences - Adrenergic Receptors (α and β) !  Alpha (α) and Beta (β)  Agonist affinity of alpha (α):  adrenaline > noradrenaline > isoprenaline  Antagonist: Phenoxybenzamine  IP3/DAG, cAMP and K+ channel opening  Agonist affinity of beta (β):  isoprenaline > adrenaline > noradrenaline  Propranolol  cAMP and Ca+ channel opening
  19. 19. Potency of catecholamines on Adrenergic Receptors Aortic strip contraction Bronchial relaxation Adr NA α β Iso Iso Adr NA Log Concentration
  20. 20. Molecular Effector Differences - α Vs β α Receptors:  IP3/DAG  cAMP  K+ channel opening β Receptors:  cAMP  Ca+ channel opening
  21. 21. Recall: Adenylyl cyclase: cAMP pathway PKA alters the functions of many Enzymes, ion channels, transporters and structural proteins. PKA Phospholamban Increased Interaction with Ca++ Faster relaxation Troponin Cardiac contractility Other Functional proteins Faster sequestration of Ca++ in SR
  22. 22. Also Recall: Phospholipase C: IP3-DAG pathway PKc
  23. 23. Beta receptors  All β receptors activate adenylate cyclase, raising the intracellular cAMP concentration  Type β1:  These are present in heart tissue, and cause an increased heart rate by acting on the cardiac pacemaker cells  Type β2:  These are in the vessels of skeletal muscle, and cause vasodilatation, which allows more blood to flow to the muscles, and reduce total peripheral resistance  Beta-2 receptors are also present in bronchial smooth muscle, and cause bronchodilatation when activated  Stimulated by adrenaline, but not noradrenaline  Bronchodilator salbutamol work by binding to and stimulating the β2 receptors  Type β3:  Beta-3 receptors are present in adipose tissue and are thought to have a role in the regulation of lipid metabolism
  24. 24. Differences between β1, β2 and β3 Beta-1 Beta-2 Beta-3 Location Heart and JG cells Bronchi, uterus, Blood vessels, liver, urinary tract, eye Adipose tissue Agonist Dobutamine Salbutamol - Antagonist Metoprolol, Atenolol Alpha-methyl propranolol - Action on NA Moderate Weak Strong
  25. 25. Clinical Effects of β-receptor stimulation  β1: Adrenaline, NA and Isoprenaline:  Tachycardia  Increased myocardial contractility  Increased Lipolysis  Increased Renin Release  β2: Adrenaline and Isoprenaline (not NA)  Bronchi – Relaxation  SM of Arterioles (skeletal Muscle) – Dilatation  Uterus – Relaxation  Skeletal Muscle – Tremor  Hypokalaemia  Hepatic Glycogenolysis and hyperlactiacidemia  β3: Increased Plasma free fatty acid – increased O2 consumption - increased heat production
  26. 26. Adrenergic receptors - alpha  Type α1  Blood vessels with alpha-1 receptors are present in the skin and the genitourinary system, and during the fight-or-flight response there is decreased blood flow to these organs  Acts by phospholipase C activation, which forms IP3 and DAG  In blood vessels these cause vasoconstriction  Type α2  These are found on pre-synaptic nerve terminals  Acts by inactivation of adenylate cyclase, cyclic AMP levels within the cell decrease (cAMP)
  27. 27. Differences between α1 and α2 Alpha-1 Alpha-2 Location Post junctional – blood vessels of skin and mucous membrane, Pilomotor muscle & sweat gland, radial muscles of Iris Prejunctional Function Stimulatory – GU, Vasoconstriction, gland secretion, Gut relaxation, Glycogenolysis Inhibition of transmitter release, vasoconstriction, decreased central symp. Outflow, platelet aggregation Agonist Phenylephrine, Methoxamine Clonidine Antagonist Prazosin Yohimbine
  28. 28. α1 adrenoceptors Clinical effects  Eye -- Mydriasis  Arterioles – Constriction (rise in BP)  Uterus -- Contraction  Skin -- Sweat  Platelet - Aggregation  Male ejaculation  Hyperkalaemia  Bladder Contraction  α2 adrenoceptors on nerve endings mediate negative feedback which inhibits noradrenaline release
  29. 29. Molecular Basis of Adrenergic Receptors Also glycogenolysis in liver Inhibition of Insulin release and Platelet aggregation Gluconeogen esis
  30. 30. Dopamine receptors  D1-receptors are post synaptic receptors located in blood vessels and CNS  D2-receptors are presynaptic present in CNS, ganglia, renal cortex
  31. 31. Summary of agents modifying adrenergic transmission Step Actions Drug Synthesis of NA Inhibition α - methyl-p-tyrosine Axonal uptake Block Cocaine, guanethidine, ephedrine Vesicular uptake Block Reserpine Vesicular NA Displacement Guanethidine Membrane NA pool Exchange diffusion Tyramine, Ephedrine Metabolism MAO-A inhibition MAO-B inhibition COMT inhibition Moclobemide Selegiline Tolcapone Receptors α 1 α 2 β1 + β2 β1 Prazosin Yohimbine Propranolol Metoprolol
  32. 32. Adrenaline as prototype  Potent stimulant of alpha and beta receptors  Complex actions on target organs
  33. 33. Heart  Beta-1 mediated action - Powerful Cardiac stimulant - +ve chronotropic, +ve inotropic  Acts on beta-1 receptors in myocardium, pacemaker cells and conducting tissue  Heart rate increases by increasing slow diastolic depolarization of cells in SAN  High doses cause marked rise in heart rate and BP causing reflex depression of SAN – unmasking of latent pacemaker cells in AVN and PF – arrhythmia (sensitization of arrhythmogenic effects by Halothane)  Cardiac systole is shorter and more powerful  Cardiac output is enhanced and Oxygen consumption is increased  Cardiac efficiency is markedly decreased  Conduction velocity in AVN, atrial muscle fibre, ventricular fibre and Bundle of His increased – benefit in partial AV block  Reduced refractory period in all cardiac cells
  34. 34. Blood Vessels  Seen mainly in the smaller vessels – arterioles – Vasoconstriction (alpha) and vasodilatation (beta) – depends on the drug  Decreased blood flow to skin and mucus membranes and renal beds – alpha effect (1 and 2) -  Increased blood flow to skeletal muscles, coronary and liver vessels - (Beta-2 effect) counterbalanced by a vasoconstrictor effect of alpha receptors
  35. 35. Blood Pressure  Depends on the Catecholamine involved  NA causes rise in Systolic, diastolic and mean BP (no beta-2 action) – unopposed alpha action  Isoprenaline causes rise in systolic but fall in diastolic BP – mean BP falls (beta-1 and beta-2)  Adr causes rise in systolic BP, but fall in diastolic BP – mean BP generally rises (slow injection)  Decreased peripheral resistance at low conc. Beta receptors are more sensitive to Adr than alpha receptors
  36. 36. Blood Pressure – contd.  Rapid IV injection of Adrenaline marked rise in Systolic and diastolic BP  Large concentration alpha action predominates – vasoconstriction even in skeletal muscle  But BP returns to normal in few minutes  A secondary fall in mean BP occurs  Mechanism – rapid uptake and dissipation of Adr – at low conc. Alpha action lost but beta action predominates – Dale`s Vasomotor reversal phenomenon
  37. 37. Dale`s Vasomotor Reversal Phenomenon
  38. 38. Actions of Adrenaline  Respiratory:  Powerful bronchodilator  Relaxes bronchial smooth muscle (not NA)  Beta-2 mediated effect  Physiological antagonist to mediators of bronchoconstriction e.g. Histamine  GIT : Relaxation of gut muscles (alpha and beta) and constricted sphincters – reduced peristalsis – not clinical importance  Bladder: relaxed detrusor muscle (beta) muscle but constriction of Trigone – both are anti-voiding effect  Uterus: Adr contracts and relaxes Uterus (alpha and beta action) but net effect depends on status of uterus and species – pregnant relaxes but non-pregnant - contracts
  39. 39. Actions of Adrenaline – contd.  Skeletal Muscle:  Facilitation of Ach release in NM junction (alpha -1)  Beta-2 acts directly on Muscle fibres  Abbreviated active state and less tension in slow conducting fibres and enhanced muscle spindle firing – tremor  CNS: No visible clinical effect in normal doses – as low penetration except restlessness, apprehension and tremor  Activation of alpha-2 in CNS decreases sympathetic outflow and reduction in BP and bradycardia - clonidine
  40. 40. Metabolic effects  Increases concentration of glucose and lactic acid  Calorigenesis (β-2 and β-3)  Inhibits insulin secretion (α-2)  Decreases uptake of glucose by peripheral tissue  Simulates glycogenolysis - Beta effect  Increases free fatty acid concentration in blood  Hypokalaemia – initial hyperkalaemia
  41. 41. ADME  All Catecholamines are ineffective orally  Absorbed slowly from subcutaneous tissue  Faster from IM site  Inhalation is locally effective  Not usually given IV  Rapidly inactivated in Liver by MAO and COMT
  42. 42. Clinical Question!  Question: A Nurse was injecting a dose of penicillin to a patient in Medicine ward without prior skin test and patient suddenly developed immediate hypersensitivity reactions. What would you do?  Answer: As the patient has developed Anaphylactic reaction, the only way to resuscitate the patient is injection of Adrenaline  0.5 mg (0.5 ml of 1:10000) IM and repeat after 5-10 minutes  Antihistaminics: Chlorpheniramine 10 – 20 mg IM or IV  Hydrocortisone 100 – 200 mg
  43. 43. Adrenaline – Clinical uses  Injectable preparations are available in dilutions 1:1000, 1:10000 and 1:100000  Usual dose is 0.3-0.5 mg sc of 1: 10000 solution  Used in:  Anaphylactic shock…  Prolong action of local anaesthetics  Cardiac arrest  Topically, to stop bleeding  Hyperkinetic children – ADHD, minimal brain dysfunction  Anorectic
  44. 44. CPR - Image
  45. 45. ADRs  Restlessness, Throbbing headache, Tremor, Palpitations  Cerebral hemorrhage, cardiac arrhythmias  Contraindicated in hypertensives, hyperthyroid and angina poctoris  Halothane and beta-blockers – not indicated
  46. 46. Other Adrenergic Drugs
  47. 47. Noradrenaline  Neurotransmitter released from postganglionic adrenergic nerve endings (80%)  Orally ineffective and poor SC absorption  IV administered Metabolized by MAO, COMT  Short duration of action
  48. 48. Actions and uses  Agonist at α1(predominant), α2 and β1 Adrenergic receptors  Equipotent with Adr on β1, but No effect on β2  Increases systolic, diastolic B.P, mean pressure, pulse pressure and stroke volume  Total peripheral resistance (TPR) increases due to vasoconstriction - Pressor agent  Increases coronary blood flow  Decreases blood flow to kidney, liver and skeletal muscles  Uses: Injection Noradrenal bitartrate slow IV infusion at the rate of 2-4mg/ minute used as a vasopressor agent in treatment of hypovolemic shock and other hypotensive states in order to raise B.P  Problems: Down regulation of receptors, Renal Vasoconstriction  Septic and neurogenic shock (?)
  49. 49. Noradrenaline - ADRs  Anxiety, palpitation, respiratory difficulty  Acute Rise of BP, headache  Extravasations causes necrosis, gangrene  Contracts gravid uterus  Severe hypertension, violent headache, photophobia, anginal pain, pallor and sweating in hyperthyroid and hypertensive patients
  50. 50. Isoprenaline  Catecholamine acting on beta-1 and beta-2 receptors – negligible action on alpha receptor  Therefore main action on Heart and muscle vasculature  Main Actions: Fall in Diastolic pressure, Bronchodilatation and relaxation of Gut  ADME: Not effective orally, sublingual and inhalation (10mg tab. SL)  Overall effect is Cardiac stimulant (beta-1)  Increase in SBP but decrease in DBP (beta-2)  Decrease in mean BP  Used as Bronchodilator and for treatment of AV block, Stokes-Adam Syndrome etc. – but not preferred anymore
  51. 51. Adrenaline, NA and Isoprenaline - Summary
  52. 52. Dopamine  Immediate metabolic precursor of Noradrenalin  High concentration in CNS - basal ganglia, limbic system and hypothalamus and also in Adrenal medulla  Central neurotransmitter, regulates body movements ineffective orally, IV use only,  Short T 1/2 (3-5minutes)
  53. 53. Dopamine MECHANISM:  Agonists at dopaminergic D1, D2 receptors  Agonist at adrenergic α1 and β1
  54. 54. Dopamine  In small doses 2-5 μg/kg/minute, it stimulates D1- receptors in renal, mesenteric and coronary vessels leading to vasodilatation (Increase in cAMP)  Recall: Renal vasoconstriction occurs in CVS shock due to sympathetic over activity  Increases renal blood flow, GFR an causes natriuresis  Interaction with D2 receptors (present in presynaptic adrenergic neurones) – suppression of NA release (no alpha effect)
  55. 55. Dopamine – cond.  Moderate dose (5-10 μg/kg/minute), stimulates β1- receptors in heart producing positive inotropic and chronotropic actions actions  Releases Noradrenaline from nerves by β1- stimulation  Does not change TPR and HR  Great Clinical benefit in CVS shock and CCF  High dose (10-30 μg/kg/minute), stimulates vascular adrenergic α1-receptors (NA release) – vasoconstriction and decreased renal blood flow
  56. 56. Why renal and mesenteric vasodilatation is useful in Shock? Increases renal blood flow, GFR an causes natriuresis In CVS shock – excessive sympathetic activity leading to ischemia of gut, sloughening and entry of Bacteria to systemic circulation - septicemia
  57. 57. Dobutamine - Derivative of Dopamine  MOA:  Acts on both alpha and beta receptors but more prominently in beta-1 receptor – increase in contractility and CO  Does not act on D1 or D2 receptors – No release of NA and thereby hypertension  Predominantly a beta-1 agonist with weak beta-2 and selective alpha-1 activity  Racemic mixture consisting of both (+) and (−) isomers - the (+) isomer is a potent β1 agonist and α1 antagonist, while the (−) isomer is an α1 agonist  Overall beta-1 activity and weak beta-2 activity  Increase in force of contraction and cardiac output but no change in heart rate  Uses: Clinically give in dose of 2-8 mcg/kg/min IV infusion in Heart failure in cardiac surgery, Septic and cardiogenic shock, Congestive Heart failure  ADRs: Tachycardia, hyperension, angina and fatal arrhythmia
  58. 58. Adrenergic agonists Selective Alpha-1 Agonists:  Phenylepherine, Ephederine, Methoxamine, Metaraminol, Mephentermine Selective Alpha-2 Agonists:  Clonidine, α-methyldopa, Guanfacine and Guanabenz Β-2 Adrenergic agonists:  Salbutamol, Terbutaline, Salmeterol, Reproterol, Oxiprenaline, Fenoterol, Isoxsuprine, Rimiterol, Ritodrine, Bitolterol and Isoetharine
  59. 59. Adrenergic Drugs – Therapeutic Classification  Pressor agents:  NA, Phenylephrine, ephedrine, Methoxamine, Dopamine  Cardiac Stimulants:  Adr, Dobutamine and Isoprenaline, Dopexamine  Nasal Decongestants:  Phenylepherine, Xylometazoline, Oxymetazoline, Naphazoline and Tetrahydrazoline and Phenylpropanolamine and Pseudoephidrine  Bronchodilators:  Isoprenaline, Salbutamol, Salmeterol, Terbutaline, Formeterol  Uterine Relaxants:  Ritodrine, Salbutamol, Isoxsuprine  Anorectics  Fenfluramine, Dexfenfluramine and Sibutramine  CNS Stimulants:  Amphetamine, Methamphetamine
  60. 60. Ephedrine  Plant alkaloid obtained from Ephedra vulgaris – Mixed acting drug (also metaraminol) – effective orally  Crosses BBB and Centrally – Increased alertness, anxiety, insomnia, tremor and nausea in adults. Sleepiness in children  Effects appear slowly but lasts longer (t1/2-4h) – 100 times less potent  Tachyphylaxis on repeated dosing (low neuronal pool)  Used as bronchodilator, mydriatic, in heart block, mucosal vasoconstriction & in myasthenia gravis  Not used commonly due to non-specific action  Uses: Mild Bronchial asthma, hypotension due to spinal anaesthesia  Available as tablets, nasal drop and injection
  61. 61. Phenylepherine - Selective, synthetic and direct α1 agonist  Actions qualitatively similar to noradrenaline  Long duration of action  Resistant to MAO and COMT  Does not cross BBB, so no CNS effects  Peripheral vasoconstriction leads to rise in BP but Reflex bradycardia  Produces mydriasis and nasal decongestion  Use:  hypovolaemic shock as pressor agent  Sinusitis & Rhinitis as nasal decongestant (common in oral preparations)  Mydriatic in the form of eye drops and lowers intraocular pressure  ADRs: Photosensitivity, conjunctival hyperemia and hypersensitivity  Administered parenteraly & topically (eye, nose)
  62. 62. What are Mucosal Decongestants?  Nasal and bronchial decongestants are the drugs used in allergic rhinitis, colds, coughs and sinusitis as nasal drops - Sympathomimetic vasoconstrictors with α- effects are used  Drugs: Phenylepherine, xylometazoline, Oxymetazoline, PPA, Pseudoephidrine etc.  Drawbacks:  Rebound congestion due to overuse  However, mucosal ischaemic damage occurs if used excessively (more often than 3 hrly) or for prolonged periods (>3weeks)  CNS Toxicity  Failure of antihypertensive therapy  Fatal hypertensive crisis in patients on MAOIs  Use only a few days since longer application reduces ciliary action
  63. 63. Nasal Decongestants  Pseudoephedrine to Ephedrine but less CNS and Cardiac effects  Poor Bronchodilator  Given in combination with antihistaminics, antitussives and NSAIDs in common cold and, allergic rhinitis, blocked Eustachian tube etc.  Rise in BP inhypertensives  Phenylpropanolamine (PPA) is similar to ephedrine and used as decongestants in many cold and cough preparations  Also as weight loosing agent  Xylometazoline, Oxymetazoline etc.
  64. 64. Amphetamine  Synthetic compound similar to Ephedrine Pharmacologically  Known because of its CNS stimulant action – psychoactive drug and also performance enhancing drug  Actions:  alertness, euphoria, talkativeness and increased work capacity – fatigue is allayed (acts on DA and NA neurotransmitters etc. –reward pathway)  increased physical performance without fatigue – short lasting (Banned drug and included in the list of drugs of “Dope Test)” – deterioration occurs  RAS Stimulation – wakefulness, sleep deprivation (then physical disability)  However, anxiety, restlessness, tremor and dysphoria occurs  Other actions: Stimulation of respiratory centre, Hunger suppression, also anticonvulsant, analgesic and antiemetic actions
  65. 65. Amphetamine – contd.  Drug of abuse – marked psychological effect but little physical dependence  Generally, Teenage abusers - thrill or kick  High Dose – Euphoria, excitement and may progress to delirium, hallucination and acute psychotic state  Also peripheral effects like arrhythmia, palpitation, vascular collapse etc.  Repeated Dose – Long term behavioural abnormalities  Starvation – acidic urine  Uses: Hyperkinetic Children (ADHD), Narcolepsy, Epilepsy and Parkinsonism
  66. 66. Anorectics  Drugs used for suppression of appetite MOA: Inhibition of NA/DA or 5-HT uptake – enhancement of monoaminergic transmission  NA agents affect the appetite centre and Serotonergics act on satiety centre  Fenfluramine, dexfenfluramine and sibutramine – ALL ARE BANNED NOW  Reasons: Heart valve defects, fibrosis and pulmonary hypertension etc.
  67. 67. Clonidine  Centrally acting: Agonist to postsynaptic α2A adrenoceptors in brain – vasomotor centre in brainstem (presynaptic Ca++ level – increased NA release)  Decrease in BP and cardiac output  Peripherally action: High dose activates peripheral presynaptic autoreceptors on adrenergic nerve ending mediating negative feedback suppression of noradrenaline release  Overdose stimulates peripheral postsynaptic α1 adrenoceptors & cause hypertension by vasoconstriction
  68. 68. Clonidine – contd.  Uses: ADHD in children, opioid withdrawal (restless legs, jitters and hypertension), alcohol withdrawal (0.3 to 0.6 mg)  Abrupt or gradual withdrawal causes rebound hypertension  Onset may be rapid (a few hours) or delayed for as long as 2 days and subsides over 2-3 days  Never use beta-blockers to treat  Available as tablets, injections and patches  Sedation, dry mouth, dizziness and constipation etc.  TCAs antagonize antihypertensive action & increase rebound hypertension of abrupt withdrawal  Low dose Clonidine (50-100μg/dl) is used in migraine prophylaxis, menopausal flushing and chorea  Moxonidine, Rilmenidine – Newer Imidazolines
  69. 69. β2 Adrenergic Agonists – discussed elsewhere!  Short acting : Salbutamol, Metaproterenol, Terbutaline, pirbuterol  Selective for β2 receptor subtype  Used for acute inhalational treatment of bronchospasm.  Onset of action within 1 to 5 minutes  Bronchodilatation lasts for 2 to 6 hours  Duration of action longer on oral administration  Directly relax airway smooth muscle  Relieve dyspnoea of asthmatic bronchoconstriction  Long acting: Salmeterol, Bitolterol, colterol
  70. 70. Uterine Relaxants - discussed elsewhere!  Antioxytocics or tocolytic agents  β2 agonists relax uterus  Used by i.v. infusion to inhibit premature labour  Isoxsuprine, Terbutaline, Ritodrine, Salbutamol  Tachycardia & hypotension occur  Use minimum fluid volume using 5% dextrose as diluents  Ritodrine: 50 μg/min, increase by 50 μg/min every 10 minutes until contractions stop or maternal heart rate is 140 beats/minute. Continue for 12-48 hours after contractions stop
  71. 71. Remember ?  Steps of Biosynthesis of Catecholamine  Distribution of adrenergic receptors  Individual Functions of Adrenergic receptors  All aspects of adrenaline – Dale`s Phenomenon  Dopamine/Dobutamine actions  Nasal decongestants - Phenylephrine  Amphetamine and Clonidine - Desirable
  72. 72. ध न य व ा द /Khuble i
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A power point presentation on Adrenergic system and Adrenergic Drugs suitable for Undergraduate MBBS level students


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