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


METHODS
Prospective, controlled, non-randomized laboratory study.


METHODS
Research laboratory.


METHODS
21 male Wistar rats.


METHODS
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.


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.
Kamel
K S
KS
Division of Nephrology, St. Michael's Hospital, Toronto, Canada.
D000138:Acidosis / Q000188:drug therapy* / Q000378:metabolism*; D000818:Animals; D002021:Buffers; D002245:Carbon Dioxide / Q000378:metabolism; D005110:Extracellular Space / Q000378:metabolism*; D006851:Hydrochloric Acid; D006863:Hydrogen-Ion Concentration; D008297:Male; D011506:Proteins / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017693:Sodium Bicarbonate / Q000627:therapeutic use*
D002021:Buffers; D011506:Proteins; D002245:Carbon Dioxide; D017693:Sodium Bicarbonate; D006851:Hydrochloric Acid