The different responses of the hepatic arterial bed to hypovolaemia and to halothane anaesthesia.

Ten dogs were subjected to a period of hypovolaemia (bleeding volume: 2% of body weight) and to a period of halothane anaesthesia (end-tidal halothane concentration: 1%). Mean arterial blood pressure decreased to 79% of control value during hypovolaemia and to 58% of control value during halothane anaesthesia. Mean total peripheral and preportal vascular resistances increased during hypovolaemia and were unchanged during halothane. Mean hepatic arterial and portal venous blood flows decreased to 82% and 55% of control values, respectively, during hypovolaemia, and to 41% and 56% of control value, respectively, during exposure to halothane. Mean hepatic arterial resistance was unchanged during hypovolaemia, but increased during halothane. Mean hepatic oxygen consumption did not change significantly during hypovolaemia, but decreased during halothane anaesthesia, in spite of an increased extraction of oxygen from both the hepatic arterial and the portal venous blood. Possible mechanisms which may maintain oxygen supply to the liver by increasing the hepatic arterial fraction of total liver blood flow when portal venous blood flow is reduced are discussed. It is concluded that this mechanism is upset or inhibited during halothane anaesthesia.