Despite the importance of oxygen in maintaining the energy requirement in renal cells and tissues, relatively little data exists on measuring renal tissue oxygen levels during the septic episode. EPR oximetry was used to measure tissue oxygen tension simultaneously in the kidney cortex and outer medulla in vivo ina mouse model of endotoxemia. Prior to injection, pO2 in the cortex region was higher compared to that in the medulla. A bolus injection of endotoxin via the tail vein resulted in a sharp drop in the cortex pO2 and an increase in the medulla pO2, resulting in a transient period of equal pO2 in both r egions. Magnetic resonance images of mouse kidneys (T2*-weighted; sensitiveto hemoglobin oxygenation) showed a sharp drop in intensity from the cortex reg ion after endotoxin injection. We have also pre-treated mice with NG-monomethly-L-arginine (to prevent nitric oxide synthesis) and found that the changes in pO2 reported above were prevented. We intend to extend these studies to further investigate the role of the various vasoactive compounds (released during theseptic episode) in altering renal blood supply and tissue oxygenation.
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