Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Division of Nephrology, Department of Medicine, Houston Methodist Hospital, Houston, Texas, USA.
Am J Nephrol. 2020;51(3):182-191. doi: 10.1159/000506274. Epub 2020 Feb 18.
We have previously investigated the fate of administered bicarbonate infused as a hypertonic solution in animals with each of the 4 chronic acid-base disorders. Those studies did not address the fate of sodium, the coadministered cation.
We examined baseline total body water (TBW), Na+ space, HCO3- space, and urinary sodium and bicarbonate excretion after acute hypertonic NaHCO3 infusion (1-N solution, 5 mmol/kg body weight) in dogs with each of the 4 chronic acid-base disorders. Observations were made at 30, 60, and 90 min postinfusion. Retained sodium that remains osmotically active distributes in an apparent space that approximates TBW. Na+ space that exceeds TBW uncovers nonosmotic sodium storage.
Na+ space approximated TBW at all times in normal and hyperbicarbonatemic animals (metabolic alkalosis and respiratory acidosis), but exceeded TBW by ~30% in hypobicarbonatemic animals (metabolic acidosis and respiratory alkalosis). Such osmotic inactivation was detected at 30 min and remained stable. The pooled data revealed that Na+ space corrected for TBW was independent of the initial blood pH but correlated with initial extracellular bicarbonate concentration (y = -0.01x + 1.4, p= 0.002). The fate of administered sodium and bicarbonate (internal distribution and urinary excretion) was closely linked.
This study demonstrates that hypobicarbonatemic animals have a Na+ space that exceeds TBW after an acute infusion of hypertonic NaHCO3 indicating osmotic inactivation of a fraction of retained sodium. In addition to an expanded Na+ space, these animals have a larger HCO3- space compared with hyperbicarbonatemic animals. Both phenomena appear to reflect the wider range of titration of nonbicarbonate buffers (Δ pH) occurring during NaHCO3- loading whenever initial [HCO3-]e is low. The data indicate that the fate of administered bicarbonate drives the internal distribution and the external disposal of sodium, the co-administered cation, and is responsible for the early, but non-progressive, osmotic inactivation of a fraction of the retained sodium.
我们之前研究了在患有 4 种慢性酸碱平衡紊乱的动物中，作为高渗溶液输注的碳酸氢盐的命运。这些研究没有涉及共同给予的阳离子钠的命运。
我们检查了在患有 4 种慢性酸碱平衡紊乱的狗中，在急性高渗碳酸氢钠输注（1-N 溶液，5 mmol/kg 体重）后基线总体液量（TBW）、Na+空间、HCO3-空间、尿钠和碳酸氢盐排泄的情况。在输注后 30、60 和 90 分钟进行观察。保留的具有渗透压活性的钠分布在近似 TBW 的表观空间中。超过 TBW 的 Na+空间揭示了非渗透性钠储存。
在正常和高碳酸氢盐血症动物（代谢性碱中毒和呼吸性酸中毒）中，Na+空间始终近似于 TBW，但在低碳酸氢盐血症动物（代谢性酸中毒和呼吸性碱中毒）中，Na+空间超过 TBW 约 30%。这种渗透压失活在 30 分钟时被检测到，并保持稳定。汇总数据显示，经 TBW 校正的 Na+空间与初始血 pH 无关，但与初始细胞外碳酸氢盐浓度相关（y=-0.01x+1.4，p=0.002）。给予的钠和碳酸氢盐的命运（内部分布和尿排泄）密切相关。
这项研究表明，在急性输注高渗碳酸氢钠后，低碳酸氢盐血症动物的 Na+空间超过 TBW，表明保留的钠的一部分发生了渗透压失活。除了扩大的 Na+空间外，这些动物的 HCO3-空间也比高碳酸氢盐血症动物大。这两种现象似乎都反映了在初始[HCO3-]e较低时，非碳酸氢盐缓冲剂的滴定范围（ΔpH）更宽，从而发生 NaHCO3-负荷。数据表明，给予的碳酸氢盐的命运驱动了共同给予的阳离子钠的内部分布和外部排泄，导致了保留的钠的一部分的早期但非进行性的渗透压失活。
