Hepatic oxygenation during arterial hypoxemia in neonatal lambs.

We identified the effects of reductions in arterial blood oxygen concentration from 15.0 to 4.0 ml O2/dl blood on hepatic blood flow, oxygen delivery, oxygen consumption and oxygen extraction in nine chronically catheterized lambs, 9 +/- 1 (SD) days of age. Hypoxemia was induced by administering a gas mixture low in oxygen to the unanesthetized lambs. Hepatic blood flow was measured with the radioactive microsphere technique; hepatic oxygen delivery, extraction, and consumption were calculated with modifications of the Fick principle. When the lambs breathed room air, hepatic blood flow was 235 +/- 30 ml/min/100 gm (mean +/- SD); hepatic oxygen delivery, 24.6 +/- 3.0 ml O2/min/100 gm; oxygen extraction, 37 +/- 11%; and hepatic oxygen consumption, 8.9 +/- 1.9 ml O2/min/100 gm. As arterial blood oxygen concentration was reduced from 15 to 6.5 ml O2/dl blood, hepatic blood flow did not change. When the concentration was less than 6.5 ml O2/dl, hepatic blood flow decreased as a result of a decrease in portal blood flow. Hepatic oxygen delivery decreased in the whole range of arterial blood oxygen concentrations studied. Despite reductions in oxygen delivery of up to 50%, hepatic oxygen consumption did not fall because hepatic oxygen extraction increased as compensation. Oxygen consumption, however, was stable only when hepatic blood flow did not change in response to hypoxemia. When hepatic blood flow fell, hepatic oxygen consumption also fell. Our data indicate that hepatic oxygen requirements can be met during hypoxemia by increases in hepatic oxygen extraction as long as hepatic blood flow does not change. When hepatic blood flow falls, hepatic oxygen consumption decreases even though oxygen reserves are still present. These data indicate that hepatic oxygenation in the neonate, as in the adult, is dependent on stable hepatic perfusion rather than adequate oxygen supply.