Hepatic
oxygen metabolism and the hepatic energy charge were assessed in 21 mongrel dogs receiving 1 to 1.5 MAC of
halothane or
thiamylal (20-30 mg.kg-1.hr-1) intravenously while inhaling graded hypoxic mixtures (FIO2 0.21-0.08). Hepatic blood flow was measured using electromagnetic flowmetry: hepatic
oxygen delivery and consumption were calculated from measured hepatic blood flow and
oxygen content in hepatic arterial, portal venous blood and hepatic venous blood. In the
hypoxia-
halothane group, portal venous blood flow (FIO2 0.15-0.10), portal venous
oxygen content (FIO2 0.10-0.08) and hepatic oxygen consumption (FIO2 0.08) significantly decreased compared with the
hypoxia-
thiamylal group. Arterial
ketone body ratio (AKBR), which indicates the mitochondrial energy charge level, decreased with the development of
hypoxia, and in the
hypoxia-
halothane group, the decrease of AKBR was significantly greater than in the
hypoxia-
thiamylal group at FIO2 0.08. The serum
catecholamine levels,
epinephrine and
norepinephrine, increased in both groups at FIO2 0.08. In the
hypoxia-
halothane group, however, the increase of
norepinephrine was significantly higher than in the
hypoxia-
thiamylal group at FIO2 0.08. These results suggest that, compared with
halothane,
thiamylal could suppress the exaggerated reaction to hypoxic
hypoxemia, maintain hepatic circulation and hepatic
oxygen metabolism and therefore maintain the hepatic mitochondrial redox state in better condition.