Renal microvascular oxygen tension during hyperoxia and acute hemodilution assessed by phosphorescence quenching and...

The kidney plays a central physiologic role as an oxygen sensor. Nevertheless, the direct mechanism by which this occurs is incompletely understood. We measured renal microvascular partial pressure of oxygen (P_kO₂) to determine the impact of clinically relevant conditions that acutely change P_kO₂ including hyperoxia and hemodilution.

We utilized two-wavelength excitation (red and blue spectrum) of the intravascular phosphorescent oxygen sensitive probe Oxyphor PdG4 to measure renal tissue PO₂ in anesthetized rats (2% isoflurane, n = 6) under two conditions of altered arterial blood oxygen content (C_aO₂): 1) hyperoxia (fractional inspired oxygen 21%, 30%, and 50%) and 2) acute hemodilutional anemia (baseline, 25% and 50% acute hemodilution). The mean arterial blood pressure (MAP), rectal temperature, arterial blood gases (ABGs), and chemistry (radiometer) were measured under each condition. Blue and red light enabled measurement of P_kO₂ in the superficial renal cortex and deeper cortical and medullary tissue, respectively.

P_kO₂ was higher in the superficial renal cortex (~ 60 mmHg, blue light) relative to the deeper renal cortex and outer medulla (~ 45 mmHg, red light). Hyperoxia resulted in a proportional increase in P_kO₂ values while hemodilution decreased microvascular P_kO₂ in a linear manner in both superficial and deeper regions of the kidney. In both cases (blue and red light), P_kO₂ correlated with C_aO₂ but not with MAP.

The observed linear relationship between C_aO₂ and P_kO₂ shows the biological function of the kidney as a quantitative sensor of anemic hypoxia and hyperoxia. A better understanding of the impact of changes in P_kO₂ may inform clinical practices to improve renal oxygen delivery and prevent acute kidney injury.