Please use this identifier to cite or link to this item:
|Title:||Furosemide reverses medullary tissue hypoxia in ovine septic acute kidney injury.|
|Authors:||Iguchi, Naoya;Lankadeva, Yugeesh R;Mori, Trevor A;Osawa, Eduardo A;Cutuli, Salvatore L;Evans, Roger G;Bellomo, Rinaldo;May, Clive N|
|Affiliation:||Preclinical Critical Care Unit, The Florey Institute of Neuroscience and Mental Health, Australia|
Department of Intensive Care, Austin Health, Heidelberg, Victoria, Australia
Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Australia
School of Medicine and Pharmacology, University of Western Australia
Univ. of Melbourne, Melbourne, Australia
|Citation:||American journal of physiology. Regulatory, integrative and comparative physiology 2019; online first: 29 May|
|Abstract:||In experimental sepsis, the rapid development of renal medullary hypoxia precedes the development of acute kidney injury (AKI) and may contribute to its pathogenesis. We investigated whether inhibiting active sodium transport and oxygen consumption in the medullary thick ascending limb with furosemide attenuates the medullary hypoxia in experimental septic AKI. Sheep were instrumented with flow probes on the pulmonary and renal arteries, and fiber optic probes to measure renal cortical and medullary perfusion and oxygen tension (PO2). Sepsis and AKI were induced by infusion of live E. coli. At 24 h of sepsis there were significant decreases in renal medullary tissue perfusion (1332±233 to 698±159 blood perfusion units) and PO2 (44±6 to 19±6 mmHg) (both p < 0.05). By 5 min after intravenous administration of furosemide (20 mg) renal medullary PO2 increased to 43±6 mmHg and remained at this normal level for 8 h. Furosemide caused transient increases in fractional excretion of sodium and creatinine clearance, but medullary perfusion, renal blood flow and renal oxygen delivery were unchanged. Urinary F2-isoprostanes, an index of oxidative stress, were not significantly changed at 24 h of sepsis, but tended to transiently decrease after furosemide treatment. In septic AKI, furosemide rapidly restored medullary PO2 to pre-septic levels. This effect was not accompanied by changes in medullary perfusion or renal oxygen delivery but was accompanied by a transient increase in fractional sodium excretion, implying decreased oxygen consumption as a mechanism.|
|Subjects:||Acute kidney injury|
|Appears in Collections:||Journal articles|
Files in This Item:
There are no files associated with this item.
Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.