Relationship of urinary and blood carbon dioxide tension during hypercapnia in the rat. Its significance in the evaluation of collecting duct hydrogen ion secretion.
Relationship of urinary and blood carbon dioxide tension during hypercapnia in the rat. Its significance in the evaluation of collecting duct hydrogen ion secretion.
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大鼠高碳酸血症期间尿液和血液二氧化碳张力的关系。
DOI：
10.1172/jci111856
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发表时间：
1985
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;Downer,M;Gutterman,C;Kurtzman,NA
本研究旨在建立急性高碳酸血症时尿pCO 2和全身血pCO 2之间的关系，并探讨这种关系对集合管氢离子（H+）分泌的意义时，尿液是酸性的，当它是高碱性的。在排泄高碱性尿液的大鼠中，血液pCO 2（从42 +/- 0.8到87 +/- 0.8 mmHg）导致尿-血（U-B）pCO 2显著下降（从31 +/- 2.0到16 +/- 4.2 mmHg，P小于0.005），这一发现可以解释为高碳酸血症抑制集合管H+分泌。与正常碳酸对照组不同，高碳酸血症大鼠的尿液pCO 2在尿液呈酸性时显著低于血液pCO 2（58 +/- 6.3和86 +/- 1.7 mmHg，P <0.001），以及在通过输注碳酸酐酶加速碳酸脱水的情况下碱化时（78 ± 2.7和87 ± 1.8 mmHg，P <0.02）。在高碳酸血症期间发现尿pCO 2低于全身血pCO 2，这表明应了解碳酸氢盐负荷前的尿pCO 2，并保持血pCO 2恒定，以使用尿pCO 2技术评价集合管H+分泌。在这些条件下进行的实验中，碳酸氢钠输注导致尿pCO 2增加（即，a Δ pCO 2），这在高碳酸血症和正常碳酸血症大鼠（分别为40 +/- 7.2和42 +/- 4.6 mmHg）中相当，而高碳酸血症和正常碳酸血症大鼠是碱性的（血液pH值分别为7.53 +/- 0.02和7.69 +/- 0.01）。然而，高碳酸血症大鼠的U-B pCO 2再次低于正常碳酸血症大鼠（分别为15 +/- 4.0和39 +/- 2.5 mmHg，P <0.001）。在碳酸氢盐输注期间不允许血液pH值变为碱性的高碳酸血症大鼠中，（7.38 +/- 0.01），Δ pCO 2高于碱血症的正常碳酸血症大鼠（分别为70 +/- 5.6和42 +/- 4.6 mmHg，P <0.005），而U-B pCO 2大致相同（39 +/- 3.7和39 +/- 2.5 mmHg）。通过测定不含碳酸酐酶的高碱性尿液和含该酶的同等碱性尿液的尿液pCO 2之间的差异，我们进一步检查了尿液pCO 2的产生。对无碱血症的高碳酸血症大鼠输注碳酸酐酶导致尿pCO（2）下降（从122+/-5.7降到77+/-2.2 mmHg），其下降幅度大于（P <0.02）碱血症的正常碳酸血症对照组（从73+/-1.9降到43+/-1.3 mmHg），且尿碳酸氢盐浓度和尿非碳酸氢盐缓冲能力相当。因此，高碳酸血症大鼠中收集粉尘H（+）分泌和滴定碳酸氢盐产生的CO（2）高于正常碳酸血症对照组。我们的结论是，在急性高碳酸血症大鼠中，碳酸氢盐负荷期间获得的U-B p（CO（2））大大低估了集合管H（+）分泌，因为它受到全身血液pCO（2）的人为影响。与U-B pCO（2）相比，Δ pCO（2）是一个更好的收集管H+分泌的定性指标，因为它不受全身血液pCO（2）的人为影响，并且它考虑了碳酸氢盐负荷前的尿PCO（2）。
This study was designed to establish the relationship between urinary pCO2 and systemic blood pCO2 during acute hypercapnia and to investigate the significance of this relationship to collecting duct hydrogen ion (H+) secretion when the urine is acid and when it is highly alkaline. In rats excreting a highly alkaline urine, an acute increase in blood pCO2 (from 42 +/- 0.8 to 87 +/- 0.8 mmHg) resulted in a significant fall in urine minus blood (U-B) pCO2 (from 31 +/- 2.0 to 16 +/- 4.2 mmHg, P less than 0.005), a finding which could be interpreted to indicate inhibition of collecting duct H+ secretion by hypercapnia. The urinary pCO2 of rats with hypercapnia, unlike that of normocapnic controls, was significantly lower than that of blood when the urine was acid (58 +/- 6.3 and 86 +/- 1.7 mmHg, P less than 0.001) and when it was alkalinized in the face of accelerated carbonic acid dehydration by infusion of carbonic anhydrase (78 +/- 2.7 and 87 +/- 1.8 mmHg, P less than 0.02). The finding of a urinary pCO2 lower than systemic blood pCO2 during hypercapnia suggested that the urine pCO2 prevailing before bicarbonate loading should be known and the blood pCO2 kept constant to evaluate collecting duct H+ secretion using the urinary pCO2 technique. In experiments performed under these conditions, sodium bicarbonate infusion resulted in an increment in urinary pCO2 (i.e., a delta pCO2) which was comparable in hypercapnic and normocapnic rats (40 +/- 7.2 and 42 +/- 4.6 mmHg, respectively) that were alkalemic (blood pH 7.53 +/- 0.02 and 7.69 +/- 0.01, respectively). The U-B pCO2, however, was again lower in hypercapnic than in normocapnic rats (15 +/- 4.0 and 39 +/- 2.5 mmHg, respectively, P less than 0.001). In hypercapnic rats in which blood pH during bicarbonate infusion was not allowed to become alkalemic (7.38 +/- 0.01), the delta pCO2 was higher than that of normocapnic rats which were alkalemic (70 +/- 5.6 and 42 +/- 4.6 mmHg, respectively, P less than 0.005) while the U-B pCO2 was about the same (39 +/- 3.7 and 39 +/- 2.5 mmHg). We further examined urine pCO2 generation by measuring the difference between the urine pCO2 of a highly alkaline urine not containing carbonic anhydrase and that of an equally alkaline urine containing this enzyme. Carbonic anhydrase infusion to hypercapnic rats that were not alkalemic resulted in a fall in urine pCO(2) (from 122+/-5.7 to 77+/-2.2 mmHg) which was greater (P <0.02) than that seen in alkalemic normocapnic controls (from 73+/- 1.9 to 43+/-1.3 mmHg) with a comparable urine bicarbonate concentration and urine nonbicarbonate buffer capacity. CO(2) generation, therefore, from collecting dust H(+) secretion and titration of bicarbonate, was higher in hypercapnic rats that in normocapnic controls. We conclude that in rats with actue hypercapnia, the U-B p(CO(2)) achieved during bicarbonate loading greatly underestimates collecting duct H(+) secretion because it is artificially influenced by systemic blood pCO(2). the deltapCO(2) is a better qualitative index of collecting duct H+ secretion that the U-B pCO(2), because it is not artificially influenced by systemic blood pCO(2) and it takes into account the urine PCO(2) prevailing before bicarbonate loading.
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