Lee Chang-Joon, Ngo Jennifer P, Kar Saptarshi, Gardiner Bruce S, Evans Roger G, Smith David W
Faculty of Engineering and Mathematical Sciences, The University of Western Australia, Perth, Western Australia, Australia.
Cardiovascular Disease Program, Biosciences Discovery Institute and Department of Physiology, Monash University, Melbourne, Sydney, Australia; and.
Am J Physiol Renal Physiol. 2017 Aug 1;313(2):F237-F253. doi: 10.1152/ajprenal.00659.2016. Epub 2017 Apr 5.
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 11 branching levels (known as "Strahler" orders) of the preglomerular renal vasculature in the rat, with an analysis of an extensive data set obtained using light microscopy to estimate oxygen mass transfer coefficients for each Strahler order. Furthermore, 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 0.4-1.4%), but increases during renal ischemia, glomerular hyperfiltration (2.1% of total renal oxygen delivery; range 0.84-3.36%), and some cardiovascular disease states (~3.0% of total renal oxygen delivery; range 1.2-4.8%). Under normal physiological conditions, blood Po 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 Po is predicted to fall most rapidly from Strahler , 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.
为了评估动静脉(AV)氧分流的生理意义,我们构建了一个新的伪三维计算模型,用于模拟氧从肾内动脉扩散至皮质组织和静脉的过程。该模型结合了大鼠肾小球前肾血管系统的11个分支水平(即“斯特拉勒”阶数),并通过光学显微镜获得的大量数据集进行分析,以估算每个斯特拉勒阶数的氧传质系数。此外,AV分流模型现在被置于一个全局氧运输模型中,该模型包括从动脉、肾小球、肾小管周围毛细血管和静脉到组织的运输。虽然有多项证据表明AV分流具有重要意义,但最重要的是,我们的AV氧分流模型预测,在正常生理条件下AV分流较小(约占肾脏总氧输送量的0.9%;范围为0.4 - 1.4%),但在肾缺血、肾小球超滤(约占肾脏总氧输送量的2.1%;范围为0.84 - 3.36%)和某些心血管疾病状态下会增加(约占肾脏总氧输送量的3.0%;范围为1.2 - 4.8%)。在正常生理条件下,预计血液氧分压从肾动脉根部到肾小球入口会下降约16 mmHg,其中AV氧分流贡献约40%,氧从动脉扩散到组织贡献约60%。在正常生理条件下,预计动脉氧分压从斯特拉勒阶数 开始下降最快。我们得出结论,AV氧分流通常对肾脏氧合的影响较小,但在肾缺血、超滤和某些心血管疾病状态下可能会加剧肾脏缺氧。