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A pseudo-three-dimensional model for quantification of oxygen diffusion from pre-glomerular arteries to renal tissue and renal venous blood

Lee, C-J, Ngo, J.P., Kar, S., Gardiner, B.S., Evans, R.G. and Smith, D.W. (2017) A pseudo-three-dimensional model for quantification of oxygen diffusion from pre-glomerular arteries to renal tissue and renal venous blood. American Journal of Physiology - Renal Physiology, 313 (2).

Link to Published Version: https://doi.org/10.1152/ajprenal.00659.2016
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Abstract

To assess the physiological significance of arterial-to-venous (AV) oxygen shunting, we generated a new pseudo-three-dimensional computational model of oxygen diffusion from intrarenal arteries to cortical tissue and veins. The model combines the eleven branching levels (known as 'Strahler' orders) of the pre-glomerular renal vasculature in the rat, with an analysis of an extensive dataset obtained using light microscopy to estimate oxygen mass transfer coefficients for each Strahler order. Further, the AV shunting model is now set within a global oxygen transport model that includes transport from arteries, glomeruli, peritubular capillaries and veins to tissue. While a number of lines of evidence suggest AV shunting is significant, most importantly our AV oxygen shunting model predicts AV shunting is small under normal physiological conditions (~0.9% of total renal oxygen delivery; range 0.4% to 1.4%), but increases during renal ischemia, glomerular hyperfiltration (~2.1% of total renal oxygen delivery; range 0.84% to 3.36%) and some cardiovascular disease states (~3.0% of total renal oxygen delivery; range 1.2% to 4.8%). Under normal physiological conditions, blood PO2 is predicted to fall by ~16 mmHg from the root of the renal artery to glomerular entry, with AV oxygen shunting contributing ~40% and oxygen diffusion from arteries to tissue contributing ~60% of this decline. Arterial PO2 is predicted to fall most rapidly from Strahler order 4, under normal physiological conditions. We conclude that AV oxygen shunting normally has only a small impact on renal oxygenation, but may exacerbate renal hypoxia during renal ischemia, hyperfiltration and some cardiovascular disease states.

Publication Type: Journal Article
Murdoch Affiliation: School of Engineering and Information Technology
Publisher: American Physiological Society
Copyright: © 2016, American Journal of Physiology-Renal Physiology
URI: http://researchrepository.murdoch.edu.au/id/eprint/38148
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