Tissue oxygen monitoring in rodent models of shock.

Tissue Po(2) (tPo(2)) reflects the balance between local O(2) supply and demand and, thus, could be a useful monitoring modality. However, the consistency and amplitude of the tPo(2) response in different organs during different cardiorespiratory insults is unknown. Therefore, we investigated the effects of endotoxemia, hemorrhage, and hypoxemia on tPo(2) measured in deep and peripheral organ beds. We compared arterial pressure, blood gas and lactate levels, descending aortic and renal blood flow, and tPo(2) in skeletal muscle, bladder epithelium, liver, and renal cortex during 1) LPS infusion (10 mg/kg), 2) sequential removal of 10% of circulating blood volume, and 3) reductions in inspired O(2) concentration in an anesthetized Wistar rat model with values measured in sham-operated animals. Different patterns were seen in each of the shock states, with condition-specific variations in the degree of acidemia, lactatemia, and tissue O(2) responses between organs. Endotoxemia resulted in a rise in bladder tPo(2) and an early fall in liver tPo(2) but no significant change in muscle and renal cortical tPo(2). Progressive hemorrhage, however, produced proportional declines in liver, muscle, and bladder tPo(2), but renal cortical tPo(2) was maintained until profound blood loss had occurred. By contrast, progressive hypoxemia resulted in proportional decreases in tPo(2) in all organ beds. This study highlights the heterogeneity of responses in different organ beds during different shock states that are likely related to local changes in O(2) supply and utilization. Whole body monitoring is not generally reflective of these changes.