Pharmacology practical Dog BP
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effect of drugs on dog blood pressure pharmacology practical.
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Pharmacology practical Dog BP
- 1. PH 4.2-Demonstrate the effects of drugs on blood pressure (vasopressor & vasodepressors with appropriate blockers) using CAL/ charts
- 2. Aim: To demonstrate the effects of various drugs (vasopressor & vasodepressors with appropriate blockers on BP & HR of perfused dog heart simulation software.
- 3. Effect of Vasopressor drugs like Epinephrine, Nor-epinephrine & Isoprenaline on BP • Epinephrine- ↑ Both BP & HR • Nor-epinephrine- ↑BP & compensatory ↓ HR • Isoprenaline- ↓ BP & ↑ HR due to + of β2 receptors.
- 5. Epinephrine (Epi)- On sudden Rapid IV injection it produced biphasic response There is marked increase BP after this it return to normal within few minute and then fall BP Initial phase- sharp ↑ in B.P due to + of α1 & β1 R. β1- increases HR & FOC ↑CO. α1-vasoconstriction blood vessels ↑ TPR ↑ BP Secondary phase- ↓ in B.P below base line is due to + of β2R vasodilation of blood vessels ↓ TPR↓ BP before normalisation. IV. Epi
- 7. Dale’s Vasomotor reversal phenomenon (due to α-blockers) When Epi. is administered after phentolamine, the effect of Epi. gets reversed & results in ↓ BP. Its due to α receptor mediated actions of Epi is blocked & exhibits only β2 receptor mediated effects i.e, vasodilation↓ BP.
- 8. Dale’s Vasomotor re- reversal phenomenon (due to b-blockers) • Epi. administered after propranolol, only rise BP observed because Epi. act only predominantly mediated via α1 receptors, beta action blocked by non selective beta blocker (propranolol). IV. Epi IV. Epi Pro
- 9. Nor-epinephrine- It cause Only sharp ↑ in BP. ↑ in B.P due to + of α1 & β1 receptors. + β1R ↑ HR & FOC ↑ CO. + α1R ↑ TPR ↑ BP.
- 11. Isoprenaline (Isoproterenol) • It decrease BP it has predominant β action cause vasodilatation but no α actions.
- 12. Vasodepressor agents Drugs like- • Cholinergic-Ach & Cholinomimetic esters • Miscellaneous-Histamine • Vasodepressors causes arteriole vasodilation via -ve inotropic or chronotropic effects that lead to ↓ systemic vascular resistance & BP. • Vasodepressors acts on specific cholinergic/ histaminic receptors to decrease BP.
- 13. Effect of vasodepressor agents like Ach & Histamine on BP • Ach-↓ both BP • Histamine- ↓ BP
- 14. Acetylcholine IV adm. of Ach causes sharp ↓in BP & quick normalisation. due to vasodilation of vascular M3R stimulation & also due to + of M2R.
- 16. Histamine • Generally causes vasodilation through H1 & H2 receptors ↓BP.
- 17. ANS: Phenomenon of Tachyphylaxis A rapid decrease in response to repeated doses over a short time period.
Editor's Notes
- MAP, or mean arterial pressure, is defined as the average pressure in a patient’s arteries during one cardiac cycle. It is considered a better indicator of perfusion to vital organs than systolic blood pressure (SBP). MAP = DBP + 1/3 PP = DBP + 1/3 (SBP –DBP) = (SBP + 2DBP) 3
- TPR- total peripheral vascular resistance Epi- Is a hormone & NT produced by adrenal glands. NE-Precursor of Epi, secrected by adrenal medulla & widespread central & automimic NT. It acts a peripheral vasoconstrictor by acting on alpha receptors. Adrenaline Activates all alpha & beta subtypes therefore a potent vasoconstrictor & cardiac stimulant Why theres’s ↑ of SBP? # +Ve chronotropic , ionotropic action on heart (beta1) # PVR (alpha1) Why there’s in DBP sometimes seen with adrenaline? # Also activates beta 2 in skeletal ms vasculature→TPR may practically fall At the height of BP there could be bradycardia (due to compensatory Vagal activity evoked by baro reflex
- Dale’s Vasomotor reversal phenomenon- Prior treatment with α blocker & followed by Adr administration causes only fall in BP instead of rise in BP due to + of spared-cardiac β1R; β2R of Sk.muscle blood vessels causes vasodilation- fall in BP by Adr. Because the β2 response is over powered, there is fall in BP. Both time use the same conc. of Adr. 10-15 min should be give gap b/w α blocker & 2nd dose of Adr to allow the antagonist to exert maximal blocking effect on Adr. receptors.
- NA- is agonist at both alpha 1 & 2 Activates beta 1 as well with same potency as Adrenaline but little effect on beta 2 ↑s PVR & DBP + SBP Compensatory baro reflex tend to overcome the direct +ve Chronotropic effect to keep HR within control but the +ve ionotropic effect on heart are maintained.
- CV effects of cholinergic agents results from both direct & indirect actions DIRECT : Heart M2 -ve chronotropic -ve ionotropic effects Result: COP INDIRECT : Blood vessels M3 EDRF release relaxation of smooth Ms vasodilatation PVR indirectly ↑s HR & COP NET EFFECT: * depend on drug concentration * small doses: BP, HR – no change * large doses: bradycardia.
- Tyramine administered Get a longer lasting pressor response than AD, NOR-AD Tyramine an indirectly acting sympathomimetic amine Nor-ad gets displaced from storage vesicle→vasoconstriction→cardiac stimulation + ↑ BP Prior administration of Tyramine hence potentiates the pressor response of catecholemines Tachyphylaxis/Acute tolerance- A/c development of tolerance after a rapid & repeated administration of a drug at shorter intervals. Due to any of the following reasons- Gradual depletion of the agonist from the storage sites with no chance of replenishment because of the repeated administration of the drug at short intervals. Ex- Tyramine, ephedrine, amphetamine. These drugs act by releasing CA from storage sites (syn’s don’t match with release) & further response decreases due to non-availability of adequate stores of CA. 2. Change in the sensitivity of target cells (P.D reason). Ex GTN (Monday disease) & LSD ( cellular adaptive tolerance).