Renal oxygen and lactate metabolism in hemorrhagic shock. An experimental study

Renal oxygen and lactate metabolism as well as central and renal hemodynamics were investigated in hemorrhagic shock in dogs. The animals were bled progressively until a 40-50% blood loss was achieved. Following a 20-, 40-, 60-, or 80-minute shock phase the shed blood was gradually returned. The effect of acute total ischemia on renal oxygen metabolism was studied during arterial occlusion. The renal cortical and medullary PO2 and PCO2 were recorded by means of implanted Silastic tonometers. The mean baseline cortical PO2 was 35 mmHg and the corresponding medullary PO2 25 mmHg. The renal cortical PO2 responded promptly to hemorrhage and declined in parallel with the cardiac output and renal blood flow. Hypoxia became more severe in the cortex than in the medulla during hemorrhagic shock. The response of both the cortical and the medullary PO2 to blood return increased with prolongation of the preceding shock phase. After one hour of shock, or more, the tissue oxygen tensions exceeded the prehemorrhage levels. Concomitantly, the renal blood flow and oxygen consumption were depressed below the initial values. The results of the studies of tissue PO2 decay curves after renal arterial occlusion suggested that the mean critical PO2 level for oxygen consumption is 15 mmHg for the cortex and 13 mmHg for the medulla. Aerobic oxidative metabolism ceased at a PO2 value of 6 mmHg in both tissue layers. In hemorrhagic shock, the critical PO2 level for oxygen consumption was reached earlier in the cortex than in the medulla. The minimum PO2 for aerobic oxidative metabolism was recorded in the cortex during severe shock, but not in the medulla. Renal lactate uptake remained rather unaffected during graded hemorrhage. The extreme impairment of renal perfusion associated with hemorrhagic shock produced a parallel decrease in the cortical PO2 and lactate utilization. Renal lactate utilization became limited at the cortical PO2 level, which coincided with the critical PO2 measured during the arterial occlusion. Lactate utilization ceased at a cortical PO2 level that was analogous with the minimum PO2 for aerobic oxidative metabolism determined after arterial occlusion. After reinfusion of shed blood renal lactate uptake failed to return to the prehemorrhage level. The renal lactate uptake was inversely related to the arterial pH under baseline conditions whereas after blood return the correlation between these parameters was less significant. The present findings suggest that in hemorrhagic shock renal metabolism may become limited by hypoxia and the susceptibility to the development of hypoxia is greater in the cortex than in the medulla.(ABSTRACT TRUNCATED AT 400 WORDS)