Adrogué H J, Brensilver J, Cohen J J, Madias N E
J Clin Invest. 1983 Apr;71(4):867-83. doi: 10.1172/jci110841.
Previous workers have shown that metabolic acidosis increases the apparent space through which administered bicarbonate is distributed. This finding has been ascribed to the accompanying acidemia and to the consequent availability of a large quantity of hydrogen ion that accumulates on nonbicarbonate tissue buffers during the development of acidosis. To test this hypothesis, bicarbonate space was measured in dogs with a broad range of steady-state plasma [HCO-3] in association with alkalemia as well as with acidemia. Appropriate combinations of pH and plasma [HCO-3] were achieved by pretreating the animals to produce graded degrees of each of the four cardinal, chronic acid-base disorders. Metabolic acidosis (n = 15) was produced by prolonged HCl-feeding; metabolic alkalosis (n = 17) by diuretics and a chloride-free diet; and respiratory acidosis (n = 9) and alkalosis (n = 8) by means of an environmental chamber. Animals with normal acid-base status (n = 4) were also studied. Sodium bicarbonate (5 mmol/kg) was infused over 10 min to the unanesthetized animals; observations were carried out over 90 min. The results obtained from animals with metabolic acid-base disturbances demonstrated an inverse relationship between bicarbonate space and initial plasma pH, confirming the previous findings of others. By contrast, the results obtained in animals with respiratory acid-base disturbances demonstrated a direct relationship between bicarbonate space and initial plasma pH. The pooled data revealed that bicarbonate space is, in fact, quite independent of the initial pH but is highly correlated with the initial level of extracellular [HCO-3]; dogs with low extracellular [HCO-3] (congruent to 10 meq/liter) whether acidemic or alkalemic, have a bicarbonate space that is 25% larger than normal and some 50% larger than in dogs with high extracellular [HCO-3] (congruent to 50 meq/liter). We conclude from these results that the increased bicarbonate space in metabolic acidosis (and respiratory alkalosis) does not reflect the availability of more hydrogen ions for release during bicarbonate administration, but merely evidences the wider range of titration (delta pH) of nonbicarbonate buffers that occurs during alkali loading whenever plasma [HCO-3] is low.
以往的研究人员已经表明，代谢性酸中毒会增加所给予的碳酸氢盐分布的表观空间。这一发现归因于伴随的酸血症以及酸中毒发展过程中在非碳酸氢盐组织缓冲液上积累的大量氢离子的可用性。为了验证这一假设，在伴有碱血症以及酸血症的情况下，对稳态血浆[HCO₃⁻]范围广泛的犬类测量了碳酸氢盐空间。通过对动物进行预处理以产生四种主要慢性酸碱紊乱中每种紊乱的不同程度，实现了pH值和血浆[HCO₃⁻]的适当组合。通过长期喂食HCl产生代谢性酸中毒（n = 15）；通过利尿剂和无氯饮食产生代谢性碱中毒（n = 17）；通过环境舱产生呼吸性酸中毒（n = 9）和碱中毒（n = 8）。还研究了酸碱状态正常的动物（n = 4）。将碳酸氢钠（5 mmol/kg）在10分钟内输注到未麻醉的动物体内；观察持续90分钟。从患有代谢性酸碱紊乱的动物获得的结果表明，碳酸氢盐空间与初始血浆pH值呈反比关系，证实了其他人先前的发现。相比之下，在患有呼吸性酸碱紊乱的动物中获得的结果表明，碳酸氢盐空间与初始血浆pH值呈正比关系。汇总的数据显示，事实上，碳酸氢盐空间与初始pH值相当独立，但与细胞外[HCO₃⁻]的初始水平高度相关；细胞外[HCO₃⁻]低（相当于10 meq/升）的犬类，无论处于酸血症还是碱血症状态，其碳酸氢盐空间比正常情况大25%，比细胞外[HCO₃⁻]高（相当于50 meq/升）的犬类大约大50%。我们从这些结果中得出结论，代谢性酸中毒（以及呼吸性碱中毒）中碳酸氢盐空间的增加并不反映在给予碳酸氢盐期间可释放的更多氢离子的可用性，而仅仅证明了每当血浆[HCO₃⁻]低时在碱负荷期间非碳酸氢盐缓冲液发生的更广泛的滴定范围（δpH）。
