THE PHARMACOLOGY OF 2-AZIRIDINYL ETHANOL

¹ Department of Pharmacology, Cornell University Medical College, New York, New York; Biochemical Research Laboratory, The Dow Chemical Company, Midland, Michigan; Department of Pharmacology, Georgetown University Schools of Medicine and Dentistry, Washington, D.C.

The pharmacology of 2-aziridinyl ethanol (2-AE) was examined in cats and in rats. 2-AE in doses greater than 5 mg/kg i.v. produces in unanesthetized cats intense fasciculations, weakness, ataxia, respiratory paralysis and death. It does not produce convulsions or signs of parasympathetic stimulation. The somatic muscle signs are caused by actions on the motor nerves. In small doses (5-10 mg/kg i.v.), 2-AE causes the neural response to a single stimulus to become repetitive, and in larger doses (ater than 10 mg/ kg.i.v. it induces long bursts of hi highfrequency spontaneous activity. The spontaneous activity is generated in the main trunk of the motor axon, and the dose of 2-AE required to produce it is inversely proportional to the length of the axon segment exposed to the drug. The activity is abolished by diphenylhydantoin and diethyl ether but is not affected by d-tubocurarine, pentobarbital or atropine. In doses greater than 40 mg/kg i.v. 2-AE causes the response of denervated muscles to a single stimulus to become repetitive. The drug has no effect on the electroencephalogram and insignificant effects on the cardiovascular system. It is very low in anticholinesterase activity. Chronic administration to rats causes splenic atrophy, lympholysis and bone marrow depression. 1-Methyl-2-aziridinyl ethanol resembles 2-AE but is less potent and is a convulsant.

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