Arruda J A, Nascimento L, Mehta P K, Rademacher D R, Sehy J T, Westenfelder C, Kurtzman N A
J Clin Invest. 1977 Oct;60(4):922-35. doi: 10.1172/JCI108847.
Measurement of urine to blood (U-B) carbon dioxide tension (P(CO2)) gradient during alkalinization of the urine has been suggested to assess distal H(+) secretion. A fact that has not been considered in previous studies dealing with urinary P(CO2) is that dissolution of HCO(3) in water results in elevation of P(CO2) which is directly proportional to the HCO(3) concentration. To investigate the interrelationship of urinary HCO(3) and urinary acidification, we measured U-B P(CO2) in (a) the presence of enhanced H(+) secretion and decreased concentrating ability i.e., chronic renal failure (CRF), (b) animals with normal H(+) secretion and decreased concentrating ability, Brattleboro (BB) rats, and (c) the presence of both impaired H(+) secretion and concentrating ability (LiCl treatment and after release of unilateral ureteral obstruction). At moderately elevated plasma HCO(3) levels (30-40 meq/liter), normal rats achieved a highly alkaline urine (urine pH > 7.8) and raised urine HCO(3) concentration and U-B P(CO2). At similar plasma HCO(3) levels, BB rats had a much higher fractional water excretion and failed to raise urine pH, urine HCO(3) concentration, and U-B P(CO2) normally. At a very high plasma HCO(3) (>50 meq/liter), BB rats raised urine pH, urine HCO(3) concentration, and U-B P(CO2) to the same levels seen in normals. CRF rats failed to raise urine pH, urine HCO(3), and U-B P(CO2) normally at moderately elevated plasma HCO(3) levels; at very high plasma HCO(3) levels, CRF rats achieved a highly alkaline urine but failed to raise U-B P(CO2). Dogs and patients with CRF were also unable to raise urine pH, urine HCO(3) concentration, and U-B P(CO2) normally at moderately elevated plasma HCO(3) levels. In rats, dogs, and man, U-B P(CO2) was directly related to urine HCO(3) concentration and inversely related to fractional water excretion. At moderately elevated plasma HCO(3) levels, animals with a distal acidification defect failed to raise U-B P(CO2); increasing the plasma HCO(3) to very high levels resulted in a significant increase in urine HCO(3) concentration and U-B P(CO2). The observed urinary P(CO2) was very close to the P(CO2) which would be expected by simple dissolution of a comparable amount of HCO(3) in water. These data demonstrate that, in highly alkaline urine, urinary P(CO2) is largely determined by concentration of urinary HCO(3) and cannot be used as solely indicating distal H(+) secretion.
有人建议通过测量尿液碱化过程中尿-血（U-B）二氧化碳分压（P(CO2)）梯度来评估远端H(+)分泌。以往关于尿P(CO2)的研究中未考虑到的一个事实是，HCO(3)在水中的溶解会导致P(CO2)升高，且与HCO(3)浓度成正比。为了研究尿HCO(3)与尿酸化之间的相互关系，我们在以下几种情况下测量了U-B P(CO2)：（a）H(+)分泌增强且浓缩能力下降，即慢性肾衰竭（CRF）；（b）H(+)分泌正常但浓缩能力下降的动物，即布拉特洛维（BB）大鼠；（c）H(+)分泌和浓缩能力均受损（LiCl处理及单侧输尿管梗阻解除后）。在血浆HCO(3)水平适度升高（30 - 40 meq/升）时，正常大鼠尿液呈高度碱性（尿pH > 7.8），尿HCO(3)浓度和U-B P(CO2)升高。在相似的血浆HCO(3)水平下，BB大鼠的水分排泄分数更高，且未能正常提高尿pH、尿HCO(3)浓度和U-B P(CO2)。在血浆HCO(3)水平非常高（>50 meq/升）时，BB大鼠的尿pH、尿HCO(3)浓度和U-B P(CO2)升高至正常大鼠的水平。CRF大鼠在血浆HCO(3)水平适度升高时，未能正常提高尿pH、尿HCO(3)和U-B P(CO2)；在血浆HCO(3)水平非常高时，CRF大鼠尿液呈高度碱性，但未能提高U-B P(CO2)。CRF犬和患者在血浆HCO(3)水平适度升高时，也无法正常提高尿pH、尿HCO(3)浓度和U-B P(CO2)。在大鼠、犬和人类中，U-B P(CO2)与尿HCO(3)浓度直接相关，与水分排泄分数呈负相关。在血浆HCO(3)水平适度升高时，存在远端酸化缺陷的动物无法提高U-B P(CO2)；将血浆HCO(3)升高至非常高的水平会导致尿HCO(3)浓度和U-B P(CO2)显著增加。观察到的尿P(CO2)非常接近通过将相当量的HCO(3)简单溶解于水中所预期的P(CO2)。这些数据表明，在高度碱性尿液中，尿P(CO2)很大程度上由尿HCO(3)浓度决定，不能仅用于指示远端H(+)分泌。
