Hepatic blood flow in phenobarbital-pretreated rats during halothane anesthesia and hypoxia

Centrilobular liver necrosis results when halothane is administered to rats pretreated with phenobarbital. Using radioactive microspheres in Wistar rats weighing 300 to 360 g each, the authors determined cardiac output and hepatic arterial and portal blood flows in normoxic (FlO2 = 0.20) unanesthetized animals pretreated with phenobarbital and in similarly pretreated animals that received halothane with adequate oxygen (FlO2 = 0.50) and while hypoxic (FlO2 = 0.08 to 0.10). Cardiac output averaged 122 +/- 8 ml/min (mean +/- SEM) in unanesthetized normoxic rats and 119 +/- 23 ml/min in unanesthetized hypoxic rats. When halothane, 0.6% in 50% oxygen, was administered cardiac output decreased significantly to 89 +/- 8 ml/min and when halothane was administered during hypoxia cardiac output was decreased further to 80 +/- 11 ml/min. During hypoxia without halothane portal venous blood flow decreased significantly but the percentages of cardiac output delivered to the hepatic artery and portal vein were not significantly different from the normoxic awake animals. When halothane was administered with adequate oxygen the percentage of the cardiac output delivered to the hepatic artery significantly increased but there was no change in absolute blood flow to either the hepatic artery or portal vein. When hypoxic animals received halothane the percentage of the cardiac output delivered to the hepatic artery and portal vein was unchanged but the absolute blood flows to the hepatic artery and portal vein decreased significantly. It is concluded that halothane combined with hypoxia is associated with changes in hepatic blood flow but that these changes are similar to changes caused by hypoxia alone. It is unlikely that hemodynamic factors account for the liver injury seen after halothane and hypoxia in phenobarbital-treated rats.