Abstract
Liver damage produced experimentally by chloroform significantly prolongs the duration of thiopentone narcosis in man. Clinical observations show that subjects with severe hepatic dysfunction require much less thiopentone to produce anæsthesia for long operations than normal subjects. A mild degree of hepatic dysfunction does not materially affect human tolerance to thiopentone. Evidence is submitted to implicate the liver as the major site for detoxication of thiopentone in man.