Journal of Applied Physiology, Vol 55, Issue 6 1748-1757, Copyright © 1983 by American Physiological Society
Ventilation and CSF ions during hypocapnic HCl and HNO3 acidosis in conscious rabbits
E. E. Nattie and G. F. Birchard
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.
