Renal venous oxygen tension as an indicator of tissue hypoxia in hemorrhagic shock.

The interrelation between the renal tissue PO2, venous PO2, oxygen consumption, and lactate utilization was investigated in dogs subjected to graded hemorrhage. The cortical PO2 measured by means of an implanted silicone elastomer tube responded immediately to graded hemorrhage. The renal venous PO2 remained at the baseline level when the cortical PO2 declined from the mean initial value of 36 to 15 torr. A further decrease in the cortical PO2 was followed by a sharp fall in the renal venous PO2, oxygen consumption, and lactate uptake. These three variables decreased simultaneously at the same cortical PO2 level. During severe hypoperfusion the renal tissue PO2 decreased progressively despite an increase in the renal arteriovenous oxygen difference. These results suggest that the renal venous PO2 remains unchanged until the tissue PO2 decreases to a level at which renal metabolism becomes limited by oxygen availability.