Journal of Applied Physiology, Vol 57, Issue 1 92-97, Copyright © 1984 by American Physiological Society
Effects of SITS, an anion transport blocker, on CSF ionic composition in metabolic alkalosis
S. Javaheri, J. Weyne, G. Demeester and I. Leusen
Disulfonic stilbenes combine with the carrier protein involved in anion
transport and inhibit the exchange of Cl- for HCO3- in a variety of
biomembranes. Our aim was to determine whether such a mechanism is
operative in the regulation of cerebrospinal fluid (CSF) [HCO3-] in
metabolic alkalosis. In anesthetized, curarized, and artificially
ventilated dogs either mock CSF (group I, 9 dogs) or mock CSF containing
SITS, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (group II, 7
dogs) was periodically injected into both lateral cerebral ventricles.
During 6 h of isocapnic metabolic alkalosis, produced by intravenous
infusion of Na2CO3 solution, plasma [HCO3-] was increased by approximately
14 meq/l in both groups. In SITS-treated animals the mean cisternal CSF
[HCO3-] increased by 7.7 meq/l after 6 h, and this was significantly higher
than the respective increment, 3.5 meq/l, noted in the control group.
Increments in CSF [HCO3-] in both groups were reciprocated by decrements in
CSF [Cl-] with CSF [Na+] remaining unchanged. Cisternal CSF PCO2 and
lactate concentrations showed similar increments in both groups. It is
hypothesized that in metabolic alkalosis a carrier transports HCO3- out of
cerebral fluid in exchange for Cl- and that SITS inhibits this mechanism.
The efflux of HCO3- out of CSF in metabolic alkalosis would minimize the
rise in CSF [HCO3-] brought about by HCO3-] influx from blood into CSF and
therefore contributes to the CSF [H+] homeostasis.
