Plummer, M.P.Lankadeva, Y.R.Finnis, M.E.Harrois, A.Harding, C.Peiris, R.M.Okazaki, N.May, C.N.Evans, R.G.Macisaac, C.M.Barge, D.Bellomo, R.Deane, A.M.2021-08-272021-08-272021Journal of Critical Care, 2021; 64:74-810883-94411557-8615http://hdl.handle.net/2440/131676Purpose: Examine effects of dexmedetomidine on bladder urinary oxygen tension (PuO₂) 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 PuO2at 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 PuO2 (−Δ 12 (7–17)mmHg). There was moderate correlation between renal medullary oxygenation and bladder PuO2; 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 PuO₂in 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.en© 2021 Elsevier Inc. All rights reserved.Dexmedetomidine; critical illness; renal; oxygenationJournal article100003955310.1016/j.jcrc.2021.03.0040006640379000132-s2.0-85103382970572257Plummer, M.P. [0000-0002-9640-1911]Finnis, M.E. [0000-0003-4125-5221]Deane, A.M. [0000-0002-7620-5577]