Urinary and renal oxygenation during dexmedetomidine infusion in critically ill adults with mechanistic insights from an ovine model
Date
2021
Authors
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.
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Journal article
Citation
Journal of Critical Care, 2021; 64:74-81
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Mark P. Plummer, Yugeesh R. Lankadeva, Mark E. Finnis, Anatole Harrois, Charlie Harding, Rachel M. Peiris, Nobuki Okazaki, Clive N. May, Roger G. Evans, Christopher M. Macisaac, Deborah Barge, Rinaldo Bellomo, Adam M. Deane
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Abstract
Purpose: 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.
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