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肾皮质中PCO2变化的分析。II. 逆流交换。

Analysis of PCO2 variations in the renal cortex. II. Countercurrent exchange.

作者信息

Atherton L J, Maddox D A, Gennari F J, Deen W M

机构信息

Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge 02139.

出版信息

Am J Physiol. 1988 Aug;255(2 Pt 2):F361-71. doi: 10.1152/ajprenal.1988.255.2.F361.

Abstract

In an effort to explain the relatively high values of CO2 partial pressure (PCO2) that have been measured in the superficial renal cortex of the rat, we developed a mathematical model based on the concept of countercurrent exchange between blood vessels. The model includes the possibility of exchange of CO2 between interlobular arteries and veins throughout the cortex, and between "terminal" arterioles and venules (those associated with the most superficial nephrons). The effect of countercurrent exchange is to amplify the increases in PCO2 that occur in the microcirculation of individual nephrons, which are due to the addition of metabolic CO2 and reabsorbed HCO3- and CO2 to peritubular capillaries. The model is formulated in terms of correlations that describe blood buffering equilibria in peritubular capillaries and in interlobular arteries and veins, and steady-state mass balances for the interlobular vessels. By use of physically reasonable vascular permeability values, simulations for the normal euvolemic Munich-Wistar rat yielded values of the surface-to-arterial PCO2 difference (delta PCO2) comparable to previously measured values. Predicted variations in delta PCO2 with afferent arteriolar blood flow rate and systemic arterial PCO2 were also in accord with available data. These results suggest that the amplifying effect of countercurrent exchange is in fact adequate to explain the high values of PCO2 measured in surface structures. The solutions to the mass balance equations are in closed analytical form and can be readily adapted to describe countercurrent exchange in the renal cortex of solutes other than CO2.

摘要

为了解释在大鼠浅表肾皮质中测得的相对较高的二氧化碳分压(PCO₂)值,我们基于血管间逆流交换的概念建立了一个数学模型。该模型考虑了整个皮质小叶间动脉和静脉之间以及“终末”小动脉和小静脉(与最浅表肾单位相关的血管)之间二氧化碳交换的可能性。逆流交换的作用是放大单个肾单位微循环中PCO₂的升高,这种升高是由于代谢产生的二氧化碳以及重吸收的HCO₃⁻和CO₂进入肾小管周围毛细血管所致。该模型依据描述肾小管周围毛细血管、小叶间动脉和静脉中血液缓冲平衡的相关性以及小叶间血管的稳态质量平衡来构建。通过使用符合生理实际的血管通透性值,对正常血容量的慕尼黑 - 威斯塔大鼠进行模拟,得到的表面与动脉PCO₂差值(δPCO₂)与先前测量值相当。预测的δPCO₂随入球小动脉血流速率和全身动脉PCO₂的变化也与现有数据相符。这些结果表明,逆流交换的放大作用实际上足以解释在浅表结构中测得的高PCO₂值。质量平衡方程的解为封闭的解析形式,并且可以很容易地用于描述肾皮质中除CO₂之外其他溶质的逆流交换。

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