Role of metabolic CO2 production in the generation of elevated renal cortical PCO2.
Role of metabolic CO2 production in the generation of elevated renal cortical PCO2.
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代谢性 CO2 产生在肾皮质 PCO2 升高中的作用。
DOI：
10.1152/ajprenal.1984.246.5.f592
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Bidani,A
中科院分区：
文献类型：
--
作者：
DuBoseJr,TD;Caflisch,CR;Bidani,A
对于在肾皮质结构中观察到的二氧化碳张力升高，人们提出了几种可能的解释。本研究旨在研究在缺乏碳酸酐酶的环境中肾脏代谢 CO2 产生和去除的贡献以及添加到管周血浆中的 CO2 不完全平衡的作用。在对照条件下以及每肾动脉高渗白蛋白、主动脉缩窄、钒酸盐、鱼藤酮或 2,4-二硝基苯酚 (2,4-DNP) 和碳酸酐酶输注后，使用 PCO2 微电极在早期 (EP) 和晚期近端 (LP) 肾小管和星状血管 (SV) 中体内测量 PCO2。在所有组中，EP、LP 和 SV 部位的 PCO2 值无法区分，但显着高于全身动脉 PCO2。使用高渗白蛋白后，PCO2 升高至 71.4 +/- 1.4 mmHg，使用 2,4-DNP 后升高至 87.0 +/- 1.8 mmHg（P 小于 0.001）。主动脉缩窄、钒酸盐输注和每肾动脉鱼藤酮治疗期间，PCO2 分别降至 53.7 +/- 0.9、55.2 +/- 2.5 和 57.3 +/- 1.3（P 小于 0.001）。鱼藤酮后肾耗氧量显着下降（-38.1 +/- 5.6 至 -13.3 +/- 2.7 mumol X min-1 X kg-1），2,4-DNP 后肾耗氧量显着增加（-35.7 +/- 5.9 至 -75.9 +/- 6.9 mumol X min-1 X kg-1）。这些发现表明，肾脏能量利用和代谢二氧化碳产生是肾皮质 PCO2 的重要来源。碳酸酐酶输注导致 PCO2 降低至 58.2 +/- 1.2 mmHg（P 小于 0.01）。（摘要截断为 250 字）
Several possible explanations for the elevated CO2 tension observed in structures of the renal cortex have been proposed. The present study was designed to investigate the contribution of renal metabolic CO2 production and removal and the role of incomplete equilibration of the CO2 added to peritubular plasma in an environment devoid of carbonic anhydrase. PCO2 was measured in vivo with PCO2 microelectrodes in early (EP) and late proximal (LP) tubules and stellate vessels (SV) during control conditions and after hyperoncotic albumin, aortic constriction, vanadate, rotenone, or 2,4-dinitrophenol (2,4-DNP) per renal artery, and carbonic anhydrase infusion. In all groups values for PCO2 in EP, LP, and SV sites were indistinguishable but significantly higher than systemic arterial PCO2. PCO2 increased to 71.4 +/- 1.4 mmHg with hyperoncotic albumin and to 87.0 +/- 1.8 mmHg after 2,4-DNP (P less than 0.001). During aortic constriction, vanadate infusion, and rotenone per renal artery, PCO2 fell to 53.7 +/- 0.9, 55.2 +/- 2.5, and 57.3 +/- 1.3, respectively (P less than 0.001). Renal O2 consumption decreased significantly after rotenone (-38.1 +/- 5.6 to -13.3 +/- 2.7 mumol X min-1 X kg-1) and increased significantly after 2,4-DNP (-35.7 +/- 5.9 to -75.9 +/- 6.9 mumol X min-1 X kg-1). These findings demonstrate that renal energy utilization and metabolic CO2 production represents an important source of renal cortical PCO2. Carbonic anhydrase infusion resulted in a decrease in PCO2 to 58.2 +/- 1.2 mmHg (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)