Role of PCO2 as determinant of CSF [HCO-3] in metabolic acidosis

Abstract

To study regulation of CSF [HCO-3] in metabolic acidosis and in particular the role of CSF PCO2 in establishing CSF bicarbonate level, acute metabolic acidosis was induced by the intravenous infusion of HCl in three groups of anesthetized dogs for six hours when PaCO2 was changed at different rates. Plasma [HCO-3] was lowered to 12 +/- 2 meq/L within one hour and maintained at that level thereafter in all groups. (I) Seven dogs were kept isocapnic while metabolic acidosis was induced. The cisternal CSF [HCO-3] fell by only 2.6 meq/L after six hours and was not significantly different from control. (II) In 11 dogs metabolic acidosis was induced while the dogs breathed spontaneously. There was a gradual drop in PaCO2 accompanied by a similar drop in CSF PCO2 of 14.5 torr. CSF [HCO-3] fell significantly by 6.1 meq/L at 6 hours and in parallel with the fall in CSF PCO2. (III) In order to show interdependence of the rate of fall in CSF [HCO-3] with rate of fall in cisternal PCO2 six dogs were mechanically hyperventilated and PaCO2 reduced to 21 torr rapidly and maintained there for six hours. CSF PCO2 followed PaCO. CSF bicarbonate fell rapidly and by 5 meq/L. In groups II and III the fall in cisternal [HCO-3] paralleled the drop in PCO2. Therefore, in metabolic acidosis the rate of the fall in cisternal bicarbonate appears to be a function of the rate of fall in CSF PCO2. It is speculated that the coupling of CSF [HCO-3] reduction in metabolic acidosis to CSF PCO2 fall is primarily for the benefit of CNS H+ homeostasis.