Neuromuscular Blocking Actions of [4,4’-Biphenylene-Bis-(2-Oxoethylene)]-Bis-[(Di-2-Ethoxyethyl) Methylammonium Bromide] ‘DEO’

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Abstract
The brief neuromuscular blocking action of [4,4’-biphenylene-bis-(2-oxoethylene) ]-bis-[(di-2-ethoxyethyl) methyl-ammonium bromide], DEO, was studied on rat sciatic nerve-gastrocnemius muscle in vivo and frog sciatic-gastrocnemius in vitro. The release of acetylcholine induced by electrical stimulation of the frog sciatic nerve was not affected by DEO at concentration of 1.3 × 10-5M which produced the neuromuscular blockade. This result indicates that DEO does not inhibit acetylcholine release nor synthesis to paralyze cholinergic neurons although it is an analog of hemicholinium. Low doses of DEO (0.1–0.3 mg/kg or 1/20–1/7 of ED50 to block the neuromuscular junction) did not affect ED50 of d-tubocurarine but enhanced the neuromuscular blocking actions of decamethonium drastically (3- to 10-fold) on rat sciatic-gastrocnemius preparation. These results suggest that the major site of action of DEO is at the junctional cholinergic receptor but not at the postjunctional ‘curare’ receptor. The LD50 of DEO determined with ICR mice was 4.45 mg/kg.

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