Renal hypoxia and lactate metabolism in hemorrhagic shock in dogs.

Abstract

Central and renal hemodynamics, renal cortical and medullary oxygen tension, and renal lactate metabolism were investigated in hemorrhagic shock in dogs. During graded hemorrhage, renal tissue PO2 decreased in parallel with renal blood flow, whereas renal lactate uptake remained virtually unchanged. During shock, below a mean arterial pressure (MAP) of 72 mm Hg, renal lactate utilization declined in parallel with tissue PO2. Renal lactate was produced at an MAP of 38 mm Hg. Reinfusion of shed blood increased renal tissue PO2 above its preshock value but did not restore baseline renal oxygen consumption and lactate uptake levels. These results suggest that renal lactate utilization is not limited by oxygen delivery under moderate hemorrhagic hypotension but decreases linearly with renal tissue PO2 during shock.