Intrarenal pO₂ measured by EPR oximetry and the effects of bacterial endotoxin

This study used Electron Paramagnetic Resonance (EPR) oximetry to detect the signal arising from oxygen-sensitive crystals of Lithium phthalocyanine (LiPC) implanted in the cortex and outer medulla of an isolated perfused rat kidney. Kidneys with implanted crystals were placed beneath the surface detector of an L-band spectrometer, and an additional gradient was induced between the poles of the magnet so as to separate the signals arising from each region, allowing simultaneous measurement of the partial pressure of oxygen (pO₂) at two locations within the same organ. In control kidneys, the pO₂ in the cortex was 96.9±7 and that of the outer medulla 11.0±4 mmHg. We found that perfusion pressure could be increased with little effect on the pO₂ of the outer medulla. At a critical point (≃140 mmHg) however, PO₂ in this region was markedly increased and was accompanied by a decrease in vascular resistance. When kidneys treated in this way were then given L-NMMA (an inhibitor of nitric oxide synthase), the pO₂ in the outer medulla returned to baseline values, presumably by blocking nitric oxide-induced vasodilation. Inclusion of Lipopolysaccharide (LPS) into the perfusion media of control kidneys resulted in a decrease in the pO₂ in the cortical region and an increase in the outer medullary region. When L-NMMA was given prior to administration of LPS, the changes in pO₂ were prevented. Based on these results, we have developed a model which can account for these observations. It indicates that re-distribution of blood (and hence oxygen) within the kidney may have an important role in altering the solute (and oxygen) gradient early during the septic episode.