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Why should we precede neostigmine by atropine in tubocurarine toxicity ?

I know that neostigmine act as anticholinesterase thus increasing the number of Ach molecules rendering them able to displace the tubocurarine, but I don't get the idea of atropine I know it's muscarinic inhibitor but we are speaking about nicotinergic receptors?

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    $\begingroup$ Please present your thoughts on the topic or at least an attempt at finding out the answer you seek. What are the actions and target sites of neostigmine and atropine? $\endgroup$ Commented May 13, 2017 at 10:22
  • $\begingroup$ I know that neostigmine act as anticholinesterase thus increasing the number of Ach molecules rendering them able to displace the tubocurarine , but I don't get the idea of atropine I know it's muscarinic inhibitor but we are speaking about N receptors $\endgroup$
    – aazz20
    Commented May 14, 2017 at 2:18

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Tubocurarine is a non-depolarising neuromuscular blocking aqgent, that is, it acts as a competetive antagonist of Acetyl Choline at the Nicotinic receptors.(Toxicity/Effect: $-N$)

Atropine is a competitive antagonist of the muscarinic acetylcholine receptor, classified as an anticholinergic. (Effect: $-M$)

Neostigmine blocks acetylcholinesterase, increasing the concentration of ACh at, and stimulating both muscarinic and nicotinic receptors. (Effect: $+M+N$)

Hence, to counter the only nicotinic deficiency of ACh, we give Neostigmine, which will also stimulate the muscarinic receptors, leading to muscarinic side effects. To counter the latter, atropine is given. A similar formulation is used in a disease like Myasthenia Gravis, with a functionally similar lesion. $$(+M+N)+(-M)+(-N)=0$$

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