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Practical pharmacology CNS

2nd year medical students Alexandria univ.

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Practical pharmacology CNS

  1. 1. 2ND YEAR MEDICAL STUDENTS MODULE IX BY DR. HAZEM ABO SHOUSHA
  2. 2. Main rules •ABP: pressure of blood on arterial wall
  3. 3. ABP= COP X PVR COP= HR X SV Main rules
  4. 4. HEART RATE Main rules
  5. 5. Main rules β1 Agonist M2 blocker β1 blocker M2 agonist HEART RATE
  6. 6. Main rules BLOOD VESSELS α1 β2 M3
  7. 7. Main rules BLOOD PRESSURE (Bl.V) VC α1 agonist β2 blocker VD α1 blocker β2 agonist M3 agonist
  8. 8. Main rules BARORECEPTORS VD VC
  9. 9. NORADRENALINE 1 1
  10. 10. Observation: increased ABP with minimal effect on HR, which increases only with high doses Explanation of effect of NE on ABP & HR:  NE acts mainly on 1 receptors  vasoconstriction PVR  With higher doses of NE, it activates also cardiac 1 receptors some increase in the heart rate
  11. 11. PRAZOSIN 1 blocker
  12. 12. What is the effect of Prazosin on ABP and HR? •it blocks 1 adrenoceptors  vasodilationPVRABP •ABP slight reflex tachycardia
  13. 13. Noradrenaline cause very minimal  in HR  β1 stimulation minimal  in BP
  14. 14. 1 β1 β2 ADRENALINE
  15. 15. Observation:  ABP & HR late The ABP  before returning to base line level Explanation of the effect of epinephrine on HR & ABP Epinephrine stimulates 1 , 1, 2 adrenoceptors Beta receptors are more sensitive to the effect of epinephrine On heart: 1 activation  +ve inotropic & chronotropic effects  COP leading to increased ABP On BV : - 1 activation vasoconstriction  PVR. - 2 activation vasodilatation  PVR
  16. 16. •The net effect of these two opposing effects (1 & 2 ) on bl.v is an in  PVR (1 wins at 1st ) •At High concentration: EPI stimulates 1 •At Low concentration: EPI stimulates 2
  17. 17. AdrenalineNoradrenalineparameters More increaseMild or no increaseHeart rate Less increase than noradrenaline More increaseBlood pressure BP decreases before reaching base line Reach base line directlyBP before Base line
  18. 18. β1 blocker Cardioselective beta blocker ATENOLOL
  19. 19. Observation: blocking 1 receptors by atenolol blocks the effect of epinephrine on HR & decreases the effect on ABP
  20. 20. block alpha1 & beta1 receptors & then inject epinephrine
  21. 21. EPINEPHRINE REVERSAL: The presser effect of epinephrine is reversed due to 1 & 1 blockade, leaving the 2 vasodilating effect acting   ABP
  22. 22. β1 + β2 blocker Non-selective beta blocker PROPRANOLOL
  23. 23. How to confirm the cause of epinephrine reversal? No epinephrine reversal since propranolol blocks not only cardiac 1 receptors but also vascular 2 receptors
  24. 24. What is the effect of propranolol on ABP and HR?
  25. 25. Propranolol mechanism as antihypertensive: 1-Block β1 in heart so low COP BP 2-  central sympathetic discharge  BP 3- Block β1 in kidney Renin  BP 4- resetting of Baroreceptors  BP 5- Block β2 presynaptic NE release  BP
  26. 26. β1 + β2 agonist Non-selective beta agonist ISOPRENALINE
  27. 27. Observation: • Isoprenaline increases HR • Isoprenaline initially decreases ABP. • As HR reaches its maximum increase, ABP shows minimal increase before returning to normal Explanation for the effect of isoprenaline on HR & ABP • Isoprenaline activates mainly beta adrenoceptor • It activates cardiac 1 receptors leading to increase in HR & force of contraction (which increases COP) • Activation of 2 receptors—Vasodilation decrease in PVR • The net effect of the two factors (COP & PVR) is a decrease in blood pressure initially. • However, when force of contraction is markedly elevated, the increase of COP overcomes the effect of decrease in PVR and thus ABP starts to increase.
  28. 28. Design an experiment to prove the explanation for the effect of Isoprenaline on HR & ABP
  29. 29. Observation: atenolol abolishes the effect of isoprenaline on HR The initial ABP-lowering effect of isoprenaline is maintained, while its pressor effect is abolished
  30. 30. PROPRANOLOL FOLLOWED BY ISOPRENALINE Observation: Propranolol blocks 1 & 2 receptors thus abolishes the effect of isoprenaline on ABP
  31. 31. 1 agonist selective Alpha agonist PHENYLEPHRINE
  32. 32. Observation: Small dose phenylephrine leads to slight increase in ABP with no effect on HR High dose phenylephrine increases markedly ABP with decrease in the HR ( reflex bradycardia)
  33. 33. Explanation of the effect of phenylephrine on ABP & HR •Activation of 1 receptors  vasoconstrictionPVR •High dose of phenylephrine  marked elevation of ABP  reflex  in sympathetic activity. Parasympathetic activity will take the upper hand  HR
  34. 34. prove the explanation of the effect of phenylephrine on HR and ABP Observation: prazosin abolishes the effect of phenylephrine on ABP & reflex bradycardia disappears
  35. 35. prove that reflex bradycardia is due to relative increase in parasympathetic activity Observation: decreased HR is abolished by atropine despite of elevation of ABP
  36. 36. Nicotinic Nn , Nm ACETYLCHOLINE ( Ach ) Muscarinic M1 , M2 ,M3
  37. 37. Observation: small doses of acetylcholine lower only ABP Higher doses produce both  in the HR & more significant lowering of ABP Explanation for the effect of acetylcholine on HR and ABP •on heart: M2 activation  - ve chronotropic effect  COP •on BV: endothelial cells M3 activation  release of NO from vascular endothelial cells  vasodilatation  PVR • Decrease in heart rate & decrease in PVR lead to  ABP
  38. 38. Inject ATROPINE & then test the effect of ACETYLCHOLINE
  39. 39. ACETYLCHOLINE REVERSAL 1. Inject a test dose of Ach 2. Inject atropine 3.Inject the same dose of acetylcholine 4.Inject a dose of Ach which is 10 times the test dose
  40. 40. Explanation for acetylcholine reversal • Atropine injection  A parasympatholytic blocks muscarinic receptors. It blocks the effect of small dose of Ach. • Ach injection [big dose]  Stimulates nicotinic receptors Nn after muscarinic receptors have been blocked by atropine   ABP • Due to activation of Nn at : • Adrenal medulla  release epinephrine  BP • Autonomic ganglia  release of catecholamines from post-synaptic adrenergic nerve endings  BP • The BP by Ach [big dose] after muscarinic receptor block [by atropine]  Ach reversal
  41. 41. oAch reversal by : Nn receptors oEPI reversal by : β2 receptors
  42. 42. Reversible anticholinesterase So  Ach ‘ ’augment Ach effect ‘ ’ NEOSTIGMINE
  43. 43. prove the mechanism of action of neostigmine

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