[Effect of ketamine on hepatic circulation and oxygen metabolism during hypoxia in dog]

The present study was designed to determine whether ketamine could maintain hepatic circulation and oxygen metabolism even in the presence of serious hepatic hypoxia. Hepatic oxygen delivery as well as consumption and the hepatic energy charge were assessed in twenty mongrel dogs receiving 30 mg.kg-1.h-1 of ketamine or thiamylal intravenously while inhaling graded hypoxic gas mixtures (FIO2 0.21 to 0.08). Hepatic blood flow was measured using electromagnetic flowmetry: hepatic oxygen delivery and consumption were calculated from hepatic blood flow and oxygen content in hepatic arterial, portal venous and hepatic venous blood. The hepatic energy charge was assessed by measuring arterial ketone body ratio (AKBR). In the ketamine group, hepatic arterial blood flow was well maintained but portal venous blood flow decreased significantly at FIO2 0.21 and 0.12 compared with thiamylal group. At FIO2 0.08, hepatic oxygen delivery, consumption and AKBR decreased significantly in the ketamine group mainly due to the decrease in oxygen delivery from portal vein, with concomitant increase in catecholamine level. These results suggest that ketamine could not suppress the exaggerated reaction to hypoxemia, and it could not maintain hepatic circulation, hepatic oxygen metabolism or hepatic mitochondrial redox state in better condition during serious hypoxemia compared with thiobarbiturate.