It has been postulated that trifluoroacetyl chloride, a halothane metabolite, can bind covalently with the phosphatidylethanolamine component of the hepatic cell membrane and cause cell necrosis. Breakdown of the necrotic hepatocyte would release N-trifluoroacetyl-ethanolamine (TFAE) into the serum with subsequent urinary excretion. An original High Performance Liquid Chromatography (HPLC) method for the measurement of TFAE is described. In six children 1 % halothane was administered for one hour and the halothane uptake measured. Urinary excretion of TFAE was measured for up to eight days and found to be 0.09 ± 0.07% or less of the absorbed halothane. In children TFAE is not a major urinary metabolite of halothane.
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Van DykeR.A., GandolfiA.J.Studies on irreversible binding of radioactivity from (14C) halothane to rat hepatic microsomal lipids and protein. Drug Metab Dispos1975; 3: 51–57.
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CohenE.N.Metabolism of halothane-2-14C in the mouse. Anesthesiology1969; 31: 560–565.
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CohenE.N., TrudellJ.R., EdmundsH.N., WatsonE.Urinary metabolites of halothane in man. Anesthesiology1975; 43: 392–401.
