Abstract

The hydrolysis of benzoylcholine, 0.05 mM, butyrylcholine, 10 mM, and suxamethonium, 0.025 mM, by the plasma of 10 subjects who developed prolonged apnoea following suxamethonium administered during anaesthesia, were measured. Plasmas from all available relatives in four families were similarly studied. The plasma of 3 subjects contained only atypical cholinesterase and hydrolysed suxamethonium, relative to butyrylcholine, at a rate of only 1.6% of that seen with usual human cholinesterase. One subject appeared to have only atypical cholinesterase on the basis of dibucaine and fluoride numbers. Suxamethonium hydrolysis, however, was sixteen times greater than that for the 3 homozygous atypical subjects. Family studies and inhibition of butrylcholine hydrolysis by decamethonium established that this subject was heterozygous with about 20% of the total cholinesterase in the usual form. Two other subjects were also heterozygous for usual and either atypical or fluoride resistant genes. One of them hydrolysed suxamethonium at 25% of the usual rate, but the other had a normal rate of suxamethonium hydrolysis. Four subjects had no detectable anomaly of plasma cholinesterase, and hydrolysed suxamethonium normally. The apparent affinity of suxamethonium for usual and atypical cholinesterase was also determined and the significance of measurements of the hydrolysis of suxamethonium in relation to prolonged apnoea produced by the drug is discussed.

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