Effects of halothane and hypoxia on hepatic oxygen metabolism in the dog.
Hepatic oxygen delivery and consumption were assessed in mongrel dogs receiving 2MAC of halothane combined with graded hypoxic hypoxemia (21-8% oxygen). 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 hypoxia-halothane group, total hepatic blood flow decreased at mild hypoxia (15% O2) from control value, but recovered to control level at moderate hypoxia (10% O2), then again decreased at 8% O2. Oxygen supply to the liver was decreased with the augmentation of hypoxia in hypoxia-halothane and hypoxia-alone groups, and it was significantly lower in the hypoxia-halothane group at 15 and 12% O2. Hepatic oxygen consumption also decreased from air control values with the increment of hypoxia, but there was no significant difference between the groups. Arterial ketone body ratio, which indicates mitochondrial energy charge level, decreased with the development of hypoxia but there was no significant difference in this ratio between the groups. These results show that halothane aggravated oxygen supply to the liver at mild to moderate hypoxia (15-12% O2), but did not worsen it specifically at more serious hypoxia (10-8% O2) compared with hypoxia alone. Hepatic hypoxia itself could not thus be a main cause of halothane hepatotoxicity.
Matsumoto
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Department of Anesthesiology, Saitama Medical School, Saitama, Japan.
Hori
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Miyazaki
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Nagasaka
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H