Renal oxygenation and lactate metabolism in hemorrhagic shock in dogs

Renal tissue oxygen tension and lactate metabolism were studied in hemorrhagic shock in dogs. The renal tissue PO2 and oxygen consumption declined in proportion to blood loss and decreasing blood flow. The decrease of tissue PO2 was greater in the cortex than in the medulla. Renal lactate uptake remained constant at the control level until 30% blood loss through an increase of renal arteriovenous lactate difference in direct proportion to arterial lactate concentration. During hemorrhagic shock after 40% blood loss lactate uptake decreased sharply and ceased almost totally. Before shock renal lactate uptake correlated highly significantly with arterial pH whereas after shock the correlation between these parameters was less significant. After reinfusions of shed blood the renal tissue PO2 returned to the prehemorrhage level in both tissue layers despite the reduced renal blood flow. At this phase renal oxygen consumption and lactate uptake failed to reach the control levels. These findings indicate that in moderate hypotension renal lactate uptake is not restricted by the local oxygen supply. During established shock tissue hypoperfusion and hypoxia seem to be responsible for deterioration of renal lactate metabolism.