Suppression of distal urinary acidification after recovery from chronic hypocapnia.
Suppression of distal urinary acidification after recovery from chronic hypocapnia.
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慢性低碳酸血症恢复后抑制远端尿酸化。
DOI：
10.1152/ajprenal.1983.245.4.f433
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Kurtzman,NA
中科院分区：
文献类型：
--
作者：
Batlle,DC;Itsarayoungyuen,K;Downer,M;Foley,R;Arruda,JA;Kurtzman,NA
本研究检测了低氧血症引起的慢性低碳酸血症恢复后不久的尿酸化。当血PCO 2恢复正常时，通过测量尿PCO 2和尿-血PCO 2差（U-B PCO 2）来评估远端酸化。在postthypocapnic大鼠，最大碱化的尿液急性碳酸氢钠负荷未能增加尿PCO 2和U-B PCO 2的水平postthypoxemic对照组大鼠和正常对照组大鼠具有可比的血液pH值和尿碳酸氢盐浓度。为了验证这一假设，即减少远端氢离子分泌的postthypocapnic大鼠导致细胞内的酸化继发于长期的低碳酸，postthypocapnic大鼠暴露于高碳酸血症的短暂持续时间（30分钟）和延长的持续时间（120分钟），试图恢复远端酸化正常。在高碳酸血症后大鼠中，短暂的高碳酸血症与尿PCO 2显著增加和尿pH值下降相关。长时间的高碳酸血症导致尿PCO 2显著增加和尿pH值进一步下降。然而，在任何尿碳酸氢盐浓度下，尿PCO_2和U-暴露于高碳酸血症的高二氧化碳血症后大鼠的B PCO 2仍显著低于同样经历长时间高碳酸血症并具有可比血液的正常对照大鼠PCO 2和血液pH值。我们的研究结果表明，远端酸化后突然恢复慢性低碳酸血症减少，如果肾脏仍然在持续的低碳酸血症的影响下。这些发现不能归因于细胞外碱血症，但可以通过假设尿酸化降低是由于细胞碱性持续存在继发于长期低碳酸血症期间产生的非CO2缓冲液的积累而导致的来解释。另外，细胞pH值以外的因素可以介导postthypocapnic大鼠远端氢离子分泌的适应性减少。
This study examined urinary acidification shortly after recovery from chronic hypocapnia induced by hypoxemia. Distal acidification was evaluated by measuring the urinary PCO2 and urine-blood PCO2 difference (U-B PCO2) when blood PCO2 had returned to normal. In posthypocapnic rats, maximal alkalinization of the urine by acute sodium bicarbonate loading failed to increase urine PCO2 and U-B PCO2 to the level of posthypoxemic control rats and normal control rats with comparable blood pH and urine bicarbonate concentration. To test the hypothesis that decreased distal hydrogen ion secretion in posthypocapnic rats resulted from intracellular alkalosis secondary to protracted hypocarbia, posthypocapnic rats were exposed to hypercapnia of brief duration (30 min) and prolonged duration (120 min) in an attempt to restore distal acidification to normal. In posthypocapnic rats, hypercapnia of brief duration was associated with a significant increase in urine PCO2 and a fall in urine pH. Prolonged hypercapnia resulted in a marked increase in urine PCO2 and a further fall in urine pH. At any urinary bicarbonate concentration, however, the urine PCO2 and U-B PCO2 posthypocapnic rats exposed to hypercapnia were still significantly lower than in normal control rats identically subjected to prolonged hypercapnia and with comparable blood PCO2 and blood pH. Our findings indicate that distal acidification after abrupt recovery from chronic hypocapnia is decreased as if the kidneys were still under the influence of sustained hypocapnia. These findings could not be ascribed to extracellular alkalemia but could be explained by postulating that decreased urinary acidification resulted from persistence of cell alkalinity secondary to the accumulation of non-CO2 buffers generated during protracted hypocarbia. Alternatively, factors other than cell pH could mediate the adaptive decrease in distal hydrogen ion secretion of posthypocapnic rats.