Batlle D C, Itsarayoungyuen K, Downer M, Foley R, Arruda J A, Kurtzman N A
Am J Physiol. 1983 Oct;245(4):F433-42. doi: 10.1152/ajprenal.1983.245.4.F433.
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.
本研究检测了低氧血症诱发的慢性低碳酸血症恢复后不久的尿液酸化情况。当血液PCO₂恢复正常时，通过测量尿液PCO₂和尿-血PCO₂差值（U-B PCO₂）来评估远端酸化。在低碳酸血症后大鼠中，急性给予碳酸氢钠负荷使尿液最大程度碱化，但未能使尿液PCO₂和U-B PCO₂升高至低氧血症后对照大鼠以及具有可比血液pH和尿液碳酸氢盐浓度的正常对照大鼠的水平。为了验证低碳酸血症后大鼠远端氢离子分泌减少是由长期低碳酸血症继发的细胞内碱中毒所致这一假说，将低碳酸血症后大鼠暴露于短时间（30分钟）和长时间（120分钟）的高碳酸血症中，试图使远端酸化恢复正常。在低碳酸血症后大鼠中，短时间高碳酸血症与尿液PCO₂显著升高及尿液pH下降有关。长时间高碳酸血症导致尿液PCO₂显著升高及尿液pH进一步下降。然而，在任何尿液碳酸氢盐浓度下，暴露于高碳酸血症的低碳酸血症后大鼠的尿液PCO₂和U-B PCO₂仍显著低于同样经历长时间高碳酸血症且具有可比血液PCO₂和血液pH的正常对照大鼠。我们的研究结果表明，慢性低碳酸血症突然恢复后的远端酸化降低，就好像肾脏仍受持续低碳酸血症的影响。这些结果不能归因于细胞外碱血症，但可以通过假设尿液酸化降低是由于长期低碳酸血症期间产生的非CO₂缓冲剂积累继发的细胞碱化持续存在来解释。或者，细胞pH以外的因素可能介导低碳酸血症后大鼠远端氢离子分泌的适应性降低。
