Sodium Fate after Sodium Bicarbonate Infusion: Influence of Altered Acid-Base Status

Am J Nephrol. 2020;51(3):182-191. doi: 10.1159/000506274. Epub 2020 Feb 18.

Abstract

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

Keywords: Bicarbonate space; Electrolytes; Osmotic inactivation; Sodium; Sodium space.

MeSH terms

  • Animals
  • Cations, Monovalent / blood
  • Cations, Monovalent / metabolism
  • Cations, Monovalent / urine
  • Disease Models, Animal
  • Dogs
  • Female
  • Humans
  • Hydrogen-Ion Concentration
  • Hypertonic Solutions
  • Infusions, Intravenous
  • Kidney
  • Renal Elimination / physiology
  • Sodium / blood
  • Sodium / metabolism*
  • Sodium / urine
  • Sodium Bicarbonate / administration & dosage
  • Sodium Bicarbonate / pharmacokinetics*
  • Tissue Distribution
  • Water-Electrolyte Imbalance / blood
  • Water-Electrolyte Imbalance / drug therapy
  • Water-Electrolyte Imbalance / metabolism*
  • Water-Electrolyte Imbalance / urine

Substances

  • Cations, Monovalent
  • Hypertonic Solutions
  • Sodium Bicarbonate
  • Sodium