[Protective effects of ulinastatin on hepatic oxygen metabolism during halothane anesthesia in the presence of graded hypoxic hypoxemia].

Hepatic oxygen metabolism and the hepatic energy charge were assessed in mongrel dogs receiving 40,000 U.kg-1 of ulinastatin intra-portally during 2 MAC halothane anesthesia combined with graded hypoxic hypoxemia (21-6% oxygen) for the purpose of evaluating the role of ulinastatin in protecting the liver against the deprivation of the hepatic energy charge resulting in halothane-induced hepatotoxicity. 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 and hepatic venous blood. In the animals who received ulinastatin during halothane anesthesia (the UST group), nine out of ten survived even at 8% oxygen, whereas six out of eight died in the halothane-alone group. There was no significant difference in total hepatic blood flow between the two groups. PaO2 was higher in the UST group than the halothane-alone group at 15 and 12% oxygen. Therefore hepatic oxygen delivery was significantly higher in the UST group at 15 and 12% oxygen. Hepatic oxygen consumption and the delivery/consumption ratio were also higher in the UST group at the various inspired oxygen levels. The arterial ketone body ratio, which indicates the mitochondrial energy charge level, significantly decreased with the progress of hypoxia in both groups, but it was significantly higher in the UST group at 8% oxygen.(ABSTRACT TRUNCATED AT 250 WORDS)