Urinary and renal oxygenation during dexmedetomidine infusion in critically ill adults with mechanistic insights from an ovine model.

PURPOSE

Examine effects of dexmedetomidine on bladder urinary oxygen tension (PuO) in critically ill patients and delineate mechanisms in an ovine model.

MATERIALS AND METHODS

In 12 critically ill patients: oxygen-sensing probe inserted in the bladder catheter and dexmedetomidine infusion at a mean (SD) rate of 0.9 ± 0.3 μg/kg/h for 24-h. In 9 sheep: implantation of flow probes around the renal and pulmonary arteries, and oxygen-sensing probes in the renal cortex, renal medulla and bladder catheter; dexmedetomidine infusion at 0.5 μg/kg/h for 4-h and 1.0 μg/kg/h for 4-h then 16 h observation.

RESULTS

In patients, dexmedetomidine decreased bladder PuOat 2 (-Δ11 (95% CI 7-16)mmHg), 8 (-Δ 7 (0.1-13)mmHg) and 24 h (-Δ 11 (0.4-21)mmHg). In sheep, dexmedetomidine at 1 μg/kg/h reduced renal medullary oxygenation (-Δ 19 (14-24)mmHg) and bladder PuO (-Δ 12 (7-17)mmHg). There was moderate correlation between renal medullary oxygenation and bladder PuO; intraclass correlation co-efficient 0.59 (0.34-0.80). Reductions in renal medullary oxygenation were associated with reductions in blood pressure, cardiac output and renal blood flow (P < 0.01).

CONCLUSIONS

Dexmedetomidine decreases PuOin critically ill patients and in sheep. In sheep this reflects a decrease in renal medullary oxygenation, associated with reductions in cardiac output, blood pressure and renal blood flow.