Bladder urine oxygen tension for assessing renal medullary oxygenation in rabbits: experimental and modeling studies.
Autor: | Sgouralis I; National Institute for Mathematical and Biological Synthesis, University of Tennessee, Knoxville, Tennessee;, Kett MM; Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Australia;, Ow CP; Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Australia;, Abdelkader A; Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Australia;, Layton AT; Department of Mathematics, Duke University, Durham, North Carolina;, Gardiner BS; School of Engineering and Information Technology, Murdoch University, Perth, Western Australia;, Smith DW; School of Computer Science and Software Engineering, The University of Western Australia, Perth, Western Australia; and., Lankadeva YR; Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria, Australia., Evans RG; Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Australia; Roger.Evans@monash.edu. |
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Jazyk: | angličtina |
Zdroj: | American journal of physiology. Regulatory, integrative and comparative physiology [Am J Physiol Regul Integr Comp Physiol] 2016 Sep 01; Vol. 311 (3), pp. R532-44. Date of Electronic Publication: 2016 Jul 06. |
DOI: | 10.1152/ajpregu.00195.2016 |
Abstrakt: | Oxygen tension (Po2) of urine in the bladder could be used to monitor risk of acute kidney injury if it varies with medullary Po2 Therefore, we examined this relationship and characterized oxygen diffusion across walls of the ureter and bladder in anesthetized rabbits. A computational model was then developed to predict medullary Po2 from bladder urine Po2 Both intravenous infusion of [Phe(2),Ile(3),Orn(8)]-vasopressin and infusion of N(G)-nitro-l-arginine reduced urinary Po2 and medullary Po2 (8-17%), yet had opposite effects on renal blood flow and urine flow. Changes in bladder urine Po2 during these stimuli correlated strongly with changes in medullary Po2 (within-rabbit r(2) = 0.87-0.90). Differences in the Po2 of saline infused into the ureter close to the kidney could be detected in the bladder, although this was diminished at lesser ureteric flow. Diffusion of oxygen across the wall of the bladder was very slow, so it was not considered in the computational model. The model predicts Po2 in the pelvic ureter (presumed to reflect medullary Po2) from known values of bladder urine Po2, urine flow, and arterial Po2 Simulations suggest that, across a physiological range of urine flow in anesthetized rabbits (0.1-0.5 ml/min for a single kidney), a change in bladder urine Po2 explains 10-50% of the change in pelvic urine/medullary Po2 Thus, it is possible to infer changes in medullary Po2 from changes in urinary Po2, so urinary Po2 may have utility as a real-time biomarker of risk of acute kidney injury. (Copyright © 2016 the American Physiological Society.) |
Databáze: | MEDLINE |
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