The effectiveness of neostigmine in the treatment of myasthenia gravis is presumably based, at least in part, on the inhibiting power of this drug on cholinesterase. By controlling the enzyme, the specific function of which is to split acetylcholine, the transmission of the nerve impulse through the synapse at the myoneural junction in sufficient amount to create an adequate response in the skeletal muscle is, according to Nachmansohn,1 thus made more certain. Similar action by other anticholinesterases, like physostigmine and strychnine, also prevents the rapid removal of the acetylcholine released during the passage of the nerve impulse. Further research has led to an investigation of some of the newer compounds known to inhibit cholinesterase, di-isopropyl-fluorophosphate (DFP), hexaethyl tetraphosphate (HETP), and tetra-ethyl pyrophosphate (TEPP).
Di-isopropyl-fluorophosphate, when given intramuscularly, definitely lowers plasma and red blood cell cholinesterase activity for long periods. Comroe2 and his associates have shown that di-isopropyl-fluorophosphate can