Acute decrease in renal microvascular Po2 during acute normovolemic hemodilution

Abstract

Large differences in the tolerance of organ systems to conditions of decreased O2 delivery such as hemodilution exist. The kidney receives ∼25% of the cardiac output and O2 delivery 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, cμPo2 and mμPo2 dropped 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 μPo2 and V̇o2ren could be observed, as well as a Po2 gap between μPo2 and PrvO2. Furthermore, there was a high correlation between V̇o2ren and 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 O2 shunt. This has clinical relevance as recent publications reporting that hemodilution during surgery forms a risk factor for postoperative renal dysfunction.