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      Measurement of Renal Tissue Oxygen Tension: Systematic Differences between Fluorescence Optode and Microelectrode Recordings in Anaesthetized Rabbits

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          Background/Aims: The validity of fluorescence optodes for measurement of renal cortical tissue oxygen tension was tested by comparison with Clark electrodes. Methods: We varied renal blood flow and inspired O<sub>2</sub> content in anaesthetized rabbits while simultaneously measuring cortical tissue oxygen tension. Results: Cortical oxygen tension varied with inspired O<sub>2</sub> content. Fluorescence optode measurements were more tightly distributed than those from a Clark electrode. Cumulative frequency distributions for fluorescence optodes were shifted to the left of those for Clark electrodes. The slope of the relationship between oxygen tension in arterial blood and cortical tissue was less for the fluorescence optode than the Clark electrode. Cortical tissue oxygen tension measurements by these two methods were correlated (r<sup>2</sup> = 0.32; p < 0.001), with no fixed bias but considerable proportional bias. Thus, the slope of the relationship between the two measurements was less than unity (0.57 [0.50–0.69]). Conclusion: Cortical oxygen tension values from fluorescence optodes are less variable but proportionally less than those from Clark electrodes. Theoretical considerations suggest that true interstitial oxygen tension lies somewhere between values provided by the two techniques. Nevertheless, the lesser variability of the fluorescence optode technique may aid detection of physiologically significant changes in intrarenal oxygenation.

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          Most cited references 17

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          Nephron pO2 and renal oxygen usage in the hypertensive rat kidney.

          The kidney has a high rate of oxygen usage (QO2) that is closely dependent on tubular Na+ transport (TNa). However, little is known concerning the regulation of the cortical partial pressure of oxygen (pO2). First, the pO2 was measured in the outer cortical proximal (PT) and distal tubules (DT), efferent arterioles (EA), and superficial (SC) and deep cortical (DC) tissues in normotensive Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHRs) using an ultramicrocoaxial O2 electrode. We next assessed the determinants of QO2 and tubular reabsorption of sodium (TNa) for whether they could account for any differences in renal cortical pO2 in SHRs. The pO2 in the EA was reduced 40 to 50% compared with arterial values but was similar in the two strains (WKY rats 45 +/- 2 vs. SHRs 41 +/- 1 mm Hg, P = NS). The pO2 value in the PT, DT, and SC did not differ within strains. All were significantly (P < 0. 001) lower in SHRs (for example, pO2 in PT of WKY rats 39 +/- 1 vs. SHRs, 30 +/- 1 mm Hg). The pO2 in the renal vein was above that at any site in the EA or the cortex, implying a precapillary shunting of O2 from the artery to vein. SHRs had reduced renal blood flow (RBF) leading to a reduced (P < 0.05) rate of O2 delivery (WKY rats 42 +/- 6 vs. SHRs 30 +/- 1 micromol. min-1. g-1) and a reduced glomerular filtration rate, leading to a lower (P < 0.001), TNa (WKYs 115 +/- 9 vs. SHRs 66 +/-8 micromol. min-1. g-1). However, despite the 43% reduction in TNa, the renal O2 usage was not significantly different between strains (WKY rats 7.6 +/- 0.8 vs. SHRs 9.0 +/- 1.0 micromol. min-1. g-1). Therefore, the SHRs had a sharp reduction (P < 0.001) in the O2 efficiency for Na+ reabsorption (TNa/QO2; WKY rats 15.1 +/- 1.6 vs. SHRs 7.3 +/-1.0 micromol-1). A precapillary O2 shunt reduces the pO2 of cortical nephrons. The pO2 is reduced further in SHRs because of less efficient O2 usage for Na+ transport.
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            Heterogeneities and profiles of oxygen pressure in brain and kidney as examples of the pO2 distribution in the living tissue.

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              Renal oxygen delivery: matching delivery to metabolic demand.

               C O’Connor (2006)
              The kidneys are second only to the heart in terms of O2 consumption; however, relative to other organs, the kidneys receive a very high blood flow and oxygen extraction in the healthy kidney is low. Despite low arterial-venous O2 extraction, the kidneys are particularly susceptible to hypoxic injury and much interest surrounds the role of renal hypoxia in the development and progression of both acute and chronic renal disease. Numerous regulatory mechanisms have been identified that act to maintain renal parenchymal oxygenation within homeostatic limits in the in vivo kidney. However, the processes by which many of these mechanisms act to modulate renal oxygenation and the factors that influence these processes remain poorly understood. A number of such mechanisms specific to the kidney are reviewed herein, including the relationship between renal blood flow and O2 consumption, pre- and post-glomerular arterial-venous O2 shunting, tubulovascular cross-talk, the differential control of regional kidney blood flow and the tubuloglomerular feedback mechanism. The roles of these mechanisms in the control of renal oxygenation, as well as how dysfunction of these mechanisms may lead to renal hypoxia, are discussed.

                Author and article information

                Nephron Physiol
                Nephron Physiology
                S. Karger AG
                March 2008
                28 January 2008
                : 108
                : 2
                : p11-p17
                aDepartment of Physiology, Monash University, Melbourne, Vic., Australia, and bDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisc., USA
                114203 Nephron Physiol 2008;108:p11
                © 2008 S. Karger AG, Basel

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                Figures: 4, References: 26, Pages: 1
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