Intrarenal oxygenation: unique challenges and the biophysical basis of homeostasis

被引:208
作者
Evans, Roger G. [1 ]
Gardiner, Bruce S. [2 ]
Smith, David W. [2 ]
O'Connor, Paul M. [3 ]
机构
[1] Monash Univ, Dept Physiol, Melbourne, Vic 3800, Australia
[2] Univ Melbourne, Dept Civil & Environm Engn, Melbourne, Vic 3010, Australia
[3] Med Coll Wisconsin, Dept Physiol, Milwaukee, WI 53226 USA
基金
英国医学研究理事会;
关键词
counter-current exchange; diffusional oxygen shunting; hyperoxia; hypoxia; kidney circulation; kidney disease;
D O I
10.1152/ajprenal.90230.2008
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Evans RG, Gardiner BS, Smith DW, O'Connor PM. Intrarenal oxygenation: unique challenges and the biophysical basis of homeostasis. Am J Physiol Renal Physiol 295: F1259-F1270, 2008. First published June 11, 2008; doi: 10.1152/ajprenal.90230.2008.-The kidney is faced with unique challenges for oxygen regulation, both because its function requires that perfusion greatly exceeds that required to meet metabolic demand and because vascular control in the kidney is dominated by mechanisms that regulate glomerular filtration and tubular reabsorption. Because tubular sodium reabsorption accounts for most oxygen consumption ((V) over dotO(2)) in the kidney, renal (V) over dotO(2) varies with glomerular filtration rate. This provides an intrinsic mechanism to match changes in oxygen delivery due to changes in renal blood flow (RBF) with changes in oxygen demand. Renal (V) over dotO(2) is low relative to supply of oxygen, but diffusional arterial-to-venous (AV) oxygen shunting provides a mechanism by which oxygen superfluous to metabolic demand can bypass the renal microcirculation. This mechanism prevents development of tissue hyperoxia and subsequent tissue oxidation that would otherwise result from the mismatch between renal (V) over dotO(2) and RBF. Recent evidence suggests that RBF-dependent changes in AV oxygen shunting may also help maintain stable tissue oxygen tension when RBF changes within the physiological range. However, AV oxygen shunting also renders the kidney susceptible to hypoxia. Given that tissue hypoxia is a hallmark of both acute renal injury and chronic renal disease, understanding the causes of tissue hypoxia is of great clinical importance. The simplistic paradigm of oxygenation depending only on the balance between local perfusion and (V) over dotO(2) is inadequate to achieve this goal. To fully understand the control of renal oxygenation, we must consider a triad of factors that regulate intrarenal oxygenation: local perfusion, local (V) over dotO(2), and AV oxygen shunting.
引用
收藏
页码:F1259 / F1270
页数:12
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