[Effects of halothane and barbiturate on hepatic circulation and hepatic oxygen metabolism during hypoxia in dogs].
ABSTRACT 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.