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Large changes in renal microvascular PO2 during acute normovolemic hemodilution


Large differences in tolerance of organ systems for conditions of decreased O2 delivery such as hemodilution exist. The kidney is an organ receiving a high amount of oxygen and is generally regarded as being less prone to reduced oxygen delivery. In a model of acute normovolemic hemodilution (ANH) we studied the total oxygenation of the rat kidney.


In 12 anesthetized and mechanically ventilated (FiO2 0.4) male Wistar rats, the arterial blood pressure (MAP) and renal blood flow (RBF) were recorded. After infusion of Oxyphor G2 the renal cortical (c) and medullary (m) microvascular PO2 (μPO2) and the renal venous PO2 were continuously measured by oxygen-dependent quenching of phosphorescence. Six animals underwent four steps of ANH (hematocrit 25%, 15%, 10% and <10%). Six animals served as time controls. Data are presented as means ± SD. P < 0.01 was considered significant.


Baseline values: RBF 6.0 ± 0.5 ml/min, cμPO2 71 ± 12 mmHg, mμPO2 53 ± 3 mmHg, DO2ren 1.4 ± 0.2 ml/min and VO2ren 0.13 ± 0.04 ml/min/g. Despite a significant increase in RBF in the first two steps of ANH (7.9 ± 2.5 and 7.5 ± 1.1 ml/min, respectively), cμPO2 and mμPO2 dropped immediately (hematocrit 25%: 37 ± 6 and 29 ± 2 mmHg; hematocrit 15%: 20 ± 4 and 15 ± 2 mmHg, respectively). VO2ren became dependent on supply when DO2ren fell below 0.5 ml/min (hematocrit 15%). With impairment of μPO2 during progressive hemodilution (lowest values cμPO2 and mμPO2 12 ± 4 and 10 ± 3 mmHg, respectively), a significant correlation between cμPO2 and m and μPO2 VO2ren could be observed (hematocrit ≤ 15%). Furthermore there was a high correlation between VO2ren and RBF over a wide range of different flows.


Our data provide evidence that the oxygen supply to the renal tissue is already becoming critical in an early stage of acute normovolemic hemodilution.


Supported by the Fortuene-Programme (No. 1168-0-0, Medical Faculty, University of Tuebingen).

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Johannes, T., Mik, E., Nohe, B. et al. Large changes in renal microvascular PO2 during acute normovolemic hemodilution. Crit Care 10 (Suppl 1), P228 (2006).

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