Ventilation and CSF ions during hypocapnic HCl and HNO3 acidosis in conscious rabbits.

In conscious rabbits with preimplanted arterial, central venous, and cisterna magna catheters, we infused HNO3 or HCl to lower and maintain arterial PCO2, pH, and plasma HCO-3 at the same mean values in both groups over 9 h. The hypothesis was that greater entry into cerebrospinal fluid (CSF) of the strong anion NO-3 vs. Cl- would result in a greater decrease in CSF [HCO-3] in the HNO3 vs. the HCl experiment, even though the acid-base stress as measured by arterial PCO2 and plasma [HCO-3] was the same. The results did not support the hypothesis. With HCl acidosis, delta CSF [HCO-3] was equal to delta CSF [Cl-]. With HNO3 acidosis, delta CSF [HCO-3] was equal to delta CSF [NO-3] + delta CSF [Cl-], as both CSF Cl- and HCO-3 decreased with NO-3 entry into CSF. The change in CSF [HCO-3] appeared tightly linked to the PCO2 or the plasma [HCO-3], it did not depend on the type of acid used. The ionic mechanisms that determine the CSF [HCO-3] in metabolic acidosis appear able to utilize changes in the strong anions NO-3 and Cl- to bring about CSF acid-base regulation. The change in alveolar ventilation per unit CO2 production as reflected by the arterial PCO2 was the same in both groups, although the expired minute ventilation and respiratory frequency responses were diminished in the HNO3 vs. the HCl groups. In both groups with acidosis, tidal volume increased, whereas respiratory frequency decreased.