The acute impact of NaHCO3 in treatment of metabolic acidosis on back-titration of non-bicarbonate buffers: a quantitative analysis.

Abstract

OBJECTIVE:

The major non-bicarbonate buffers are intracellular proteins, a detrimental effect of severe acidosis could be their titration with H+. This in turn would lead to their net charge becoming more positive, and possibly, to changes in their shape and function. Since NaHCO3 is a treatment option in patients with severe metabolic acidosis, the purpose of this study was to examine the acute effect of the administration of NaHCO3 on back-titration of non-bicarbonate buffers in metabolic acidosis.

DESIGN:

Prospective, controlled, non-randomized laboratory study.

SETTING:

Research laboratory.

SUBJECTS:

21 male Wistar rats.

INTERVENTION:

Rats were anesthetized, intubated and ventilated. Ventilation was adjusted at the beginning of the experiment to a PCO2 of approximately 30 mmHg, no further adjustments were made thereafter. Acute metabolic acidosis was induced by the infusion of 3.5 mmol of hydrochloric acid over 1 hour. After an equilibration period, 3 groups of seven rats were studied; group I received 0.75 mmol NaHCO3, group II received equimolar NaCl, and group III served as time control.

MEASUREMENTS AND MAIN RESULTS:

Measurements were made to enable quantitation of how much HCO3 was retained in the ECF and how much was titrated with H+ and was excreted as "acid-base" CO2. Since there are so few H+ present in the ECF in a free or a bound form, and in the absence of an increase in endogenous acid-production, the source of this H+ is from proteins in the ICF. As compared to the NaCl and the time control groups, the administration of NaHCO3 led to significant alkalinization of the ECF, pH rose from 7.22 +/- 0.03 to 7.34 +/- 0.02. Of the 0.75 mmol of NaHCO3 that was administered, 67% or 0.52 +/- 0.08 mmol was retained in ECF. Only a small amount (0.07 +/- 0.09 mmol) of acid-base CO2 was excreted.

CONCLUSIONS:

The administration of NaHCO3 does not acutely lead to a significant back-titration of non-bicarbonate buffers, especially under conditions of fixed ventilation.

• Authors: K S Kamel
• Journal: Clinical nephrology (Clin Nephrol) Vol. 45 Issue 1 Pg. 51-5 (Jan 1996) ISSN: 0301-0430 [Print] Germany
• PMID: 8616957 (Publication Type: Comparative Study, Journal Article)

Chemical References

• Buffers
• Proteins
• Carbon Dioxide
• Sodium Bicarbonate
• Hydrochloric Acid

Topics

• Acidosis (drug therapy, metabolism)
• Animals
• Buffers
• Carbon Dioxide (metabolism)
• Extracellular Space (metabolism)
• Hydrochloric Acid
• Hydrogen-Ion Concentration
• Male
• Proteins (metabolism)
• Rats
• Rats, Wistar
• Sodium Bicarbonate (therapeutic use)