Hepatic gluconeogenesis during halothane anaesthesia in man.

It is known that hepatic gluconeogenesis from lactate and aminoacids is inhibited by halothane in in vitro studies on isolated, perfused livers. In the present work, the effect of halothane anaesthesia on hepatic gluconeogenesis was studied in three volunteers during a constant amino-acid infusion and compared with three control subjects who did not receive any halothane during the amino-acid infusion. Prior to the investigation, all the subjects were on a carbohydrate-poor diet in order to deplete hepatic glucogen stores. During the investigation, hepatic gluconeogenesis was stimulated by a constant amino-acid infusion which caused a slight rise in total hepatic blood flow (THBF), a marked increase in splanchnic oxygen consumption and oxygen extraction, elevation in blood glucose and urea levels and in splanchnic glucose and urea releases. Halothane anaesthesia administered during continued amino-acid infusion caused a reduction in THBF to sub-control values, while the increased oxygen consumption was only slightly reduced, thereby further increasing splanchnic oxygen extraction. Blood glucose and urea levels of the anaesthetized subjects were consistent with those of the control subjects. Splanchnic release of glucose was reduced almost to control values during halothane. However, the release of urea was only slightly reduced. It is concluded that the stimulating effect on hepatic gluconeogenesis caused by the amino-acid infusion was inhibited during halothane anaesthesia, while metabolization of the amino-acids, other than through gluconeogenesis, proceeded without any major changes.