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氯耗竭性碱中毒时集合管各节段的碳酸氢盐转运

Bicarbonate transport in collecting duct segments during chloride-depletion alkalosis.

作者信息

Galla J H, Rome L, Luke R G

机构信息

Department of Internal Medicine, University of Cincinnati Medical Center, Ohio, USA.

出版信息

Kidney Int. 1995 Jul;48(1):52-5. doi: 10.1038/ki.1995.266.

Abstract

Renal correction of chloride-depletion alkalosis (CDA) by chloride replacement results in bicarbonate secretion in the cortical collecting duct (CD) and urinary bicarbonate excretion. To assess the participation of the more distal segments of the CD, we determined net total CO2 transport in the outer medullary (OMCD), initial (IMCDi) and terminal (IMCDt) inner medullary CD segments obtained from Sprague-Dawley rats with normal acid-base balance (NML) or with CDA produced by peritoneal dialysis. Tubules were bathed and perfused with isotonic solutions containing Cl 110 mM and HCO, 25 mM. Net total CO2 transport was decreased in all segments: OMCD 22.1 +/- 4.2 to 9.2 +/- 2.0; IMCDi 38.1 +/- 4.6 to 9.3 +/- 1.7; IMCDt 6.7 +/- 1.2 to -0.5 +/- 0.4 pmol/min/mm tubule length. Perfusion rates, tubule lengths, and transepithelial voltages did not differ between groups in any segment. These data show that all CD segments beyond the cortical segment decrease bicarbonate reabsorption during CDA. This permits the bicarbonate secreted by the cortical CD to be excreted, and is likely an important mechanism for the correction of CDA.

摘要

通过补充氯离子对氯耗竭性碱中毒(CDA)进行肾脏纠正,会导致皮质集合管(CD)分泌碳酸氢盐并经尿液排出。为了评估集合管更远端节段的作用,我们测定了从酸碱平衡正常(NML)或因腹膜透析导致CDA的Sprague-Dawley大鼠获取的外髓质集合管(OMCD)、初始内髓质集合管(IMCDi)和终末内髓质集合管(IMCDt)节段的总二氧化碳净转运量。肾小管用含有110 mM Cl和25 mM HCO的等渗溶液进行灌流和浸泡。所有节段的总二氧化碳净转运量均降低:OMCD从22.1±4.2降至9.2±2.0;IMCDi从38.1±4.6降至9.3±1.7;IMCDt从6.7±1.2降至-0.5±0.4 pmol/分钟/毫米肾小管长度。各组间任何节段的灌注速率、肾小管长度和跨上皮电压均无差异。这些数据表明,在CDA期间,皮质节段以外的所有集合管节段都会减少碳酸氢盐的重吸收。这使得皮质集合管分泌的碳酸氢盐得以排出,这可能是纠正CDA的一个重要机制。

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