Reversal of renal tissue hypoxia during experimental cardiopulmonary bypass in sheep by increased pump flow and arterial pressure

Abstract

Aim: Renal tissue hypoxia during cardiopulmonary bypass could contribute to the pathophysiology of acute kidney injury. We tested whether renal tissue hypoxia can be alleviated during cardiopulmonary bypass by the combined increase in target pump flow and mean arterial pressure.

Methods: Cardiopulmonary bypass was established in eight instrumented sheep under isoflurane anaesthesia, at a target continuous pump flow of 80 mL·kg^-1 min^-1 and mean arterial pressure of 65 mmHg. We then tested the effects of simultaneously increasing target pump flow to 104 mL·kg^-1 min^-1 and mean arterial pressure to 80 mmHg with metaraminol (total dose 0.25-3.75 mg). We also tested the effects of transitioning from continuous flow to partially pulsatile flow (pulse pressure ~15 mmHg).

Results: Compared with conscious sheep, at the lower target pump flow and mean arterial pressure, cardiopulmonary bypass was accompanied by reduced renal blood flow (6.8 ± 1.2 to 1.95 ± 0.76 mL·min^-1 kg^-1) and renal oxygen delivery (0.91 ± 0.18 to 0.24 ± 0.11 mL·O₂ min^-1 kg^-1). There were profound reductions in cortical oxygen tension (PO₂) (33 ± 13 to 6 ± 6 mmHg) and medullary PO₂ (31 ± 12 to 8 ± 8 mmHg). Increasing target pump flow and mean arterial pressure increased renal blood flow (to 2.6 ± 1.0 mL·min^-1 kg^-1) and renal oxygen delivery (to 0.32 ± 0.13 mL·O₂ min^-1kg^-1) and returned cortical PO₂ to 58 ± 60 mmHg and medullary PO₂ to 28 ± 16 mmHg; levels similar to those of conscious sheep. Partially pulsatile pump flow had no significant effects on renal perfusion or oxygenation.

Conclusions: Renal hypoxia during experimental CPB can be corrected by increasing target pump flow and mean arterial pressure within a clinically feasible range.

Keywords: acute kidney injury; cardiopulmonary bypass; pulsatile pump flow; renal blood flow; renal oxygenation; renal perfusion.