Does the administration of carbicarb lead acutely to back-titration of non-bicarbonate buffers ?

Objecrive : We have recently demonstrated in a model of acute metabolic acidosis in rats that the administration of NaHCO 3 does not lead acutely to back-titration of non-bicarbonate buffers. Carbicarb is a new alkalinizing agent that has been proposed as a replacement for NaHCO 3 in the treatment of metabolic acidosis. Hence, the purpose of this study was to examine the impact of carbicarb on back-titration of non-bicarbonate buffers. Methods : Rats were anaesthetized, intubated and ventilated to a P Co2 of 30 mmHg. Acute metabolic acidosis was induced by the infusion over 1 hour of 3.5 mmol of hydrochloric acid. After a 20 min equilibration period, 3 groups of rats (n = 7 in each group) were examined. Rats in group I received 0.75 meq of Na from 1 M carbicarb solution as an intravenous bolus, rats in group II received equimolar NaCl, while rats in group III were used as time controls. Calculations were performed to quantitate the amount of HCO 3 - that was retained in the ECF volume and the amount that was titrated with H + and excreted as acid-base CO 2 . Acid-base CO 2 was considered as the amount of CO 2 that was excreted in excess of what would be produced during metabolism. Results : As compared to the NaCl and the time control groups, the administration of carbicarb led to significant alkalinization of the ECF, pH rose from 7.23 ± 0.02 to 7.34 ± 0.03. Of the 0.75 mmol of carbicarb that was administered, 0.61 ± 0.05 mmol (70%) was retained in ECF. There was virtually no acid-base CO 2 produced. Conclusions : The administration of carbicarb does not lead acutely to back-titration of non-bicarbonate buffers especially under conditions of fixed ventilation.