Journal of Applied Physiology, Vol 61, Issue 2 633-639, Copyright © 1986 by American Physiological Society
Cerebrospinal fluid ions in metabolic acidosis in dogs: effects of acetazolamide
S. Javaheri, J. Kennealy, C. D. Runck, R. G. Loudon, M. B. Pine and R. E. Myers
We hypothesized that, during isosmotic isonatremic HCl acidosis with
maintained isocapnia in cisternal cerebrospinal fluid (CSF), acetazolamide,
by inhibiting carbonic anhydrase (CA) in the central nervous system (CNS),
should produce an isonatric hyperchloric metabolic acidosis in CSF. Blood
and CSF ions and acid-base variables were measured in two groups of
anesthetized and paralyzed dogs with bilateral ligation of renal pedicles
during 5 h of HCl acidosis (plasma [HCO3-] = 11 meq/l). Mechanical
ventilation was regulated such that arterial PCO2 dropped and CSF Pco2
remained relatively constant. In group I (control group, n = 6), CSF [Na+]
remained unchanged, [HCO3-] and strong ions difference (SID) fell,
respectively, 6.1 and 5 meq/l, and [Cl-] rose 3.5 meq/l after 5 h of
acidosis. In acetazolamide-treated animals, (group II, n = 7), CSF [Na+]
remained unchanged, [HCO3-], and SID fell 11 and 7.1 meq/l, respectively,
and [Cl-] rose 7.1 meq/l. We conclude that during HCl acidosis inhibition
of CNS CA by acetazolamide induces an isonatric hyperchloric metabolic
acidosis in CSF, which is more severe than that observed in controls.
