experimental pharmacology practical

1. Effect of various drug on dogs BP

23. Viva questions
• What do you understand by potentiation? Example.
• What do you mean by additive effect?
• Explain synergism with example?

24. • Potentiation- Effect of combination is greater than the
individual effects of the components. In these case when
one component given alone produces no effect, but
enhances the effect of the other.(1+0 >1)
 Levodopa + Carbidopa
 Amoxycillin+ Clavulanic acid
• Additive effect/Summation- The effect of 2 drugs is in the
same direction & simply adds up.(1+1=2). If different MOA
then summation & if by same mechanism then addition.
 Amlodipine+ Atenolol
 Aspirin+ Paracetamol
• Synergism- If combined effect of 2 drugs is having similar
action is more than the algebraic sum of their individual
effect(1+1>2). Eg.sulfamethoxazole+ trimethoprim

25. • What is antagonism?
• Types of antagonism?
• Clinical significance of drug antagonism?
• What is mixed agonist- antagonist? Example.

26. • Antagonism- when one drug decreases or abolishes the
action of others.
• Types-
 Physical – Charcoal adsorbs alkaloids
 Chemical- KMnO4 oxidizes alkaloids, Chelating agents
 Physiological/ Functional- Histamine & adrenaline
 Receptor- One drug blocks the receptor action of the other.
 Competitive receptor antagonism
 Non- competitive receptor antagonism
• Clinical significance-
T/t of certain conditions & poisonings-
 Use of antacids in peptic ulcer(Chemical antagonism)
 Adrenaline in anaphylactic shock(Physiological antagonism)
 Poisoning(Naloxone in opioid poisoning)

27. To overcome or reduce the adverse effect of a drug e.g use
of benzhexol with trifluoperazine to reduce EPS.
• Mixed agonist- antagonist- Agonist at some receptor &
antagonist at some receptors e.g- buprenorphine,
butorphanol, pentazocine, nalbuphine.

28. Tachyphylaxis
• Identify the drug A?
• What is the phenomena called & mechanism
involved?
• Can you overcome this by-
a) Increasing the dose of A.
b) Increasing the time interval between doses.

29. • Indirectly acting sympathomimetic- Tyramine.
• Phenomena is tachyphylaxis i.e rapid development of
acute tolerance with quick succession.
• The mechanism involved here is pharmacodynamic
tolerance d/t sensitization or down regulation of receptors.
• Tyramine acts by displacing NE from the vesicles in the
adrenergic neurons, thus releasing more & more NE which
acts on the receptors in the synaptic cleft to produce
hypertensive crisis. The synthesis of NE is not able to match
the release & stores get depleted. So, after some times less
amount of NE is available for action on receptors in the
synaptic cleft. Also vesicle is now occupied by octapamine
produced from tyramine which on release has no action on
adrenergic receptors. Hence, BP goes on decreasing further.

30. • This can’t be overcome by increasing the dose
of tyramine, bcoz it has no action on the α
receptors on synaptic cleft.
• Increasing the time interval between doses
may be helpful becoz the receptors won’t get
downregulated & NE is not displaced
completely at a time.

32. • Effect on BP-
• A NE, increase in SBP, DBP as well as mean BP.
• B E, increase in SBP d/t alpha action & fall in DBP d/t
beta action.
• C isoprenaline, rise in SBP but marked fall in DBP.(beta 1-
myocardial stimulation, beta 2- vasodilatation)
• Effect on TPR-
• A increases PVR d/t alpha action
• B decreases PVR d/t vasodilatory beta 2 action
• C marked decrease in PVR d/t beta 2 action.

33. THANK YOU