Neostigmine is a drug that helps nerve impulses get to muscles.
It works at the neuromuscular junction, preventing the neurotransmitter 'acetylcholine' from being broken down by the enzyme 'cholinesterase'. As it increases the amount of acetylcholine around, it facilitates stimulation of both nicotinic and muscarinic receptors. This means it also helps parasympathetic signals get to the heart (It's a cholinergic parasympathomimetic agent). The parasympathetic input to the heart happens to encourage it to slow down. (In contrast to the sympathetic input which speeds it up). If you want to avoid this second effect (the bradycardia), you could administer atropine (or preferably, glycopyrronium) at the same time.
The main use for neostigmine is after anaesthesia, in order to reverse the action of non-depolarising muscle relaxants such as atracurium or vecuronium. It is NOT used to reverse the depolarising muscle relaxant 'suxamethonium', it would actually enhance the effects of suxamethonium. Neostigmine can be used to help diagnose and treat myasthenia gravis, as demonstrated by Mary Walker of London in 1935, and to treat curare poisoning.
Side effects of neostigmine due to its muscarinic effects are: nausea, vomiting, colic, excessive salivation, diarrhoea and bradycardia.
Overdose can actually cause a depolarising nerve block, causing paralysis in a similar way to suxamethonium. Other signs of neostigmine overdose include bronchoconstriction, excessive sweating, and nystagmus.
This drug should not be used in intestinal or urinary obstruction, and extreme caution should be used in asthma.
It can be taken orally, 15 - 30 mg at a time, for alleviation of the symptoms of myasthenia gravis, and can last four hours. It is given i.v. for reversal of neuromuscular block, the dose being 50-70 micrograms/kg (max 5mg). In this context, it is given over one minute with atropine or glycopyrronium, acts within a minute, and lasts 20 - 30 minutes.
The effects of neostigmine are reduced by propranolol or lithium.