Oxygen and carbon dioxide tensions in the canine kidney during arterial occlusion and hemorrhagic hypotension.

Renal cortical and medullary tissue pO2 and pCO2 were measured by means of implanted Silastic tonometers during arterial occlusion and graded hemorrhage in dogs. The results of studies of tissue pO2 decay curves after interruption of renal circulation suggest that a mean critical pO2 level for oxygen consumption is 15 millimeters of mercury for the cortex and 13 millimeters of mercury for the medulla. Aerobic oxidative metabolism ceased at a pO2 value of 6 millimeters of mercury in both tissue layers. At this phase, carbon dioxide was produced anaerobically in both tissue layers. In graded hemorrhage, the critical pO2 level for oxygen consumption and the minimum pO2 value for aerobic oxidative metabolism were reached earlier in the cortex than in the medulla, which may contribute to the frequent occurrence of ischemic damage and necrosis in the renal cortex after severe hemorrhagic shock.