Although sedatives are frequently required in the treatment of patients with liver disease, barbiturates are believed to be contraindicated in the face of impaired hepatic function. Three points are advanced in support of this belief: First, patients with advanced liver disease have remained comatose for long periods of time after receiving a barbiturate; second, animals after chloroform induced hepatic damage or partial liver extirpation have shown an increased sensitivity to anesthetic doses of barbiturates (1, 2); and third, animals are alleged to show a greater than normal retention of pentobarbital and barbital in their blood and tissues after chloroform anesthesia (3). These points of evidence, however, are far 'from conclusive. The natural progression of hepatic coma from a stage of restlessness to one of somnolence, and the spontateous fluctuations that occur in the course of liver disease reduce the significance of temporal correlations in determining the part any single factor plays in causing hepatic coma. As far as animal experiments are concerned, they are not necessarily applicable to man, particularly if the type of liver damage and the barbiturate dosage are not comparable to the usual clinical situation. Finally, methods of barbiturate analysis are difficult and non-specific. Since the evidence incriminating the use of barbiturates in liver disease seemed circumstantial, a study to obtain direct evidence was undertaken. Three questions in particular seemed worthy of consideration:

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