Large differences in the tolerance of organ systems to conditions of decreased O2delivery such as hemodilution exist. The kidney receives ∼25% of the cardiac output and O2delivery is in excess of the oxygen demand under normal circumstances. In a rat model of acute normovolemic hemodilution (ANH), we studied the effect of reduced hematocrit on renal regional and microvascular oxygenation. Experiments were performed in 12 anesthetized male Wistar rats. Six animals underwent four steps of ANH (hematocrit 25, 15, 10, and <10%). Six animals served as time-matched controls. Systemic and renal hemodynamic and oxygenation parameters were monitored. Renal cortical (c) and outer medullary (m) microvascular PO2(μPO2) and the renal venous PO2(PrvO2) were continuously measured by oxygen-dependent quenching of phosphorescence. Despite a significant increase in renal blood flow in the first two steps of ANH, cμPO2and mμPO2dropped immediately. From the first step onward oxygen consumption (V̇O2ren) became dependent on oxygen delivery (DO2ren). With a progressive decrease in hematocrit, a significant correlation between μPO2and V̇O2rencould be observed, as well as a PO2gap between μPO2and PrvO2. Furthermore, there was a high correlation between V̇O2renand RBF over a wide range of flows. In conclusion, the oxygen supply to the renal tissue is becoming critical already in an early stage of ANH due to the combination of increased V̇O2ren, decreased DO2ren, and intrarenal O2shunt. This has clinical relevance as recent publications reporting that hemodilution during surgery forms a risk factor for postoperative renal dysfunction. Copyright

Kidney, Oxygen consumption, Phosphorescence quenching, Renal microvascular oxygenation, Tissue oxygenation,
American Journal of Physiology - Renal Fluid and Electrolyte Physiology
Erasmus MC: University Medical Center Rotterdam

Johannes, T, Mik, E.G, Nohé, B, Unertl, K.E, & Ince, C. (2007). Acute decrease in renal microvascular PO2 during acute normovolemic hemodilution. American Journal of Physiology - Renal Fluid and Electrolyte Physiology, 292(2). doi:10.1152/ajprenal.00206.2006