Renal Oxygen Delivery and Consumption during Progressive Hypoxemia in the Anesthetized Dog

Abstract

The relationship between renal oxygen delivery (RDO₂) and function was evaluated during progressive hypoxemia. Seven anesthetized, spontaneously breathing dogs were given progressively lower oxygen concentrations to breathe while monitoring renal O₂ consumption (RVO₂), renal hemodynamic and excretory function. In addition, basal RVO₂ was determined in three models of kidneys without filtration. RDO₂ averaged 3648 μmole O₂/min/100 g during normoxia. Basal RVO₂ averaged 100 μmole O₂/min/100 g kidney while total RVO₂ was 466 μmole O₂/min/100 g kidney during normoxia, leaving 366 μmole O₂/min/100 g consumed by those processes involved in tubular transport. During hypoxemia, all renal parameters were well maintained until the lowest P _aO₂ (24.2 Torr). At this level, total RVO₂ and RDO₂ were significantly reduced. However, RDO₂ remained well above RVO₂ throughout hypoxemia. The reduction in RVO₂ was a direct result of decreased O₂ demand, as glomerular filtration and tubular load were also reduced. This associated decrease in O₂ demand and RVO₂ was indicated by the fact that the renal (a - v)O₂ difference remained low and unchanged (1.9 vol%), fractional sodium excretion was unchanged, and the ratio of tubular sodium reabsorption to RVO₂ also remained unchanged (30.8 meq Na/mmole O₂). It was concluded that hypoxemia, while reducing both RDO₂ and RVO₂ at the lowest P _aO₂ (24.2 Torr), did not functionally impair renal excretory function by limiting RDO₂ to the tubular transport processes. A reduction in RBF is far more likely to compromise the RDO₂ needed to sustain basal and active transport processes than hypoxemia itself.