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Tissue oxygen monitoring in rodent models of shock

Bloomsbury Institute of Intensive Care Medicine, Department of Medicine, and Wolfson Institute for Biomedical Research, University College London, London, United Kingdom

Submitted 15 January 2007 ; accepted in final form 19 March 2007

Tissue PO₂ (tPO₂) reflects the balance between local O₂ supply and demand and, thus, could be a useful monitoring modality. However, the consistency and amplitude of the tPO₂ response in different organs during different cardiorespiratory insults is unknown. Therefore, we investigated the effects of endotoxemia, hemorrhage, and hypoxemia on tPO₂ measured in deep and peripheral organ beds. We compared arterial pressure, blood gas and lactate levels, descending aortic and renal blood flow, and tPO₂ 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 O₂ 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 O₂ responses between organs. Endotoxemia resulted in a rise in bladder tPO₂ and an early fall in liver tPO₂ but no significant change in muscle and renal cortical tPO₂. Progressive hemorrhage, however, produced proportional declines in liver, muscle, and bladder tPO₂, but renal cortical tPO₂ was maintained until profound blood loss had occurred. By contrast, progressive hypoxemia resulted in proportional decreases in tPO₂ 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 O₂ supply and utilization. Whole body monitoring is not generally reflective of these changes.

tissue oxygen tension; hemodynamics; rat; endotoxemia; hemorrhage; hypoxemia