Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/19175
Title: Intrarenal and urinary oxygenation during norepinephrine resuscitation in ovine septic acute kidney injury.
Austin Authors: Lankadeva, Yugeesh R;Kosaka, Junko;Evans, Roger G;Bailey, Simon R;Bellomo, Rinaldo ;May, Clive N
Affiliation: Cardiovascular Disease Program, Bioscience Discovery Institute and Department of Physiology, Monash University, Melbourne, Victoria, Australia
Faculty of Veterinary Science, University of Melbourne, Melbourne, Victoria, Australia
The Australian and New Zealand Intensive Care Research Centre, Melbourne, Victoria, Australia
The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Victoria, Australia
Department of Intensive Care, Austin Health, Heidelberg, Victoria, Australia
Department of Medicine, Austin Health, Heidelberg, Victoria, Australia
Issue Date: Jul-2016
metadata.dc.date: 2016-04-16
Publication information: Kidney International 2016; 90(1): 100-8
Abstract: Norepinephrine is the principal vasopressor used to restore blood pressure in sepsis, but its effects on intrarenal oxygenation are unknown. To clarify this, we examined renal cortical, medullary, and urinary oxygenation in ovine septic acute kidney injury and the response to resuscitation with norepinephrine. A renal artery flow probe and fiberoptic probes were placed in the cortex and medulla of sheep to measure tissue perfusion and oxygenation. A probe in the bladder catheter measured urinary oxygenation. Sepsis was induced in conscious sheep by infusion of Escherichia coli for 32 hours. At 24 to 30 hours of sepsis, either norepinephrine, to restore mean arterial pressure to preseptic levels or vehicle-saline was infused (8 sheep per group). Septic acute kidney injury was characterized by a reduction in blood pressure of ∼12 mm Hg, renal hyperperfusion, and oliguria. Sepsis reduced medullary perfusion (from an average of 1289 to 628 blood perfusion units), medullary oxygenation (from 32 to 16 mm Hg), and urinary oxygenation (from 36 to 24 mm Hg). Restoring blood pressure with norepinephrine further reduced medullary perfusion to an average of 331 blood perfusion units, medullary oxygenation to 8 mm Hg and urinary oxygenation to 18 mm Hg. Cortical perfusion and oxygenation were preserved. Thus, renal medullary hypoxia caused by intrarenal blood flow redistribution may contribute to the development of septic acute kidney injury, and resuscitation of blood pressure with norepinephrine exacerbates medullary hypoxia. The parallel changes in medullary and urinary oxygenation suggest that urinary oxygenation may be a useful real-time biomarker for risk of acute kidney injury.
URI: http://ahro.austin.org.au/austinjspui/handle/1/19175
DOI: 10.1016/j.kint.2016.02.017
ORCID: 0000-0002-1650-8939
PubMed URL: 27165831
Type: Journal Article
Subjects: cortical and medullary tissue oxygenation
cortical and medullary tissue perfusion
hypoxia
norepinephrine
renal blood flow
sepsis
Appears in Collections:Journal articles

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