Pyridostigmine reversal

A principle of the therapy for acute poisonings with OPC lies in the complex performance of cholinolytics (atropine, scopolamine, aprofene, amisile etc.) with reversible ChE inhibitors (pyridostigmine, proserine etc.) or cholinolytics with tranquillizers (diazepam, fenozepame etc)... 

The failure of physostigmine to reverse BZ effects during the first 8 hours (Fig. 8) is interesting and unexplained. It reminds one of the Berry and Davies findings (in 1970 at the British labs in Porton Down) which showed that the reversible anticholinesterase pyridostigmine was paradoxically effective as a prophylactic agent in the event of nerve gas exposure (see ref. ). 

The pharmacological properties of ambenonium are similar to neostigmine and pyridostigmine, and it works by reversible inactivation of cholinesterase. A synonym of this drug is ambenonium. 

Reversal of neuromuscular blockade Adults and children, 0.2 mg for each 1 mg neostigmine or 5 mg pyridostigmine. Administer IV simultaneously. 

A third approach to protection against excessive acetylcholinesterase inhibition is pretreatment with reversible enzyme inhibitors to prevent binding of the irreversible organophosphate inhibitor. This prophylaxis can be achieved with pyridostigmine but is reserved for situations in which possibly lethal poisoning is anticipated, eg, chemical warfare (see Chapter 7). Simultaneous use of atropine is required to control muscarinic excess. 

Pyridostigmine Mestinon Myasthenia gravis, reversal of neuromuscular blocking drugs... 

Acetylcholinesterase inhibitors can probably be safely used in pregnancy when needed, provided the dosage is carefully regulated. Reversible muscle weakness in a newborn infant was attributed to relative overdosage of the mother with pyridostigmine bromide (11). 

Pyridostigmine bromide competitively binds to nerve tissue AchE. The binding is reversible and has been shown to protect AchE against irreversible inhibition by organophosphorus nerve agents. Pyridostigmine is a quarternary compound and does not readily cross the blood-brain barrier. Thus, it is not expected to affect or protect brain AchE. Cholinesterase inhibition, which is a mechanism of action, is also responsible for toxicity. 

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