Dilution acidosis: evidence for a role of intracellular ph in the
control of ventilation.
Kasserra, C. E., and D. R. Jones.
Dept. of Zoology, University of British Columbia, Vancouver, B.C.,
Canada V6T 1Z4
APStracts 2:0493A, 1995.
Acute hyperosmolality results in an extracellular dilution acidosis
and hypercarbia that does not stimulate ventilatory compensation. The
osmotic stress is also associated with shifts in water and
electrolyte balance, and an increase in intracellular pH. The
alkaline intracellular pH was hypothesized to have a role in
preventing a normal respiratory response to the extracellular
acidosis and hypercarbia. Therefore, this study examined the effect
of ion-exchange blockade on intra- and extracellular pH and
ventilation during acute hyperosmolality in the Pekin duck (Anas
platyrhynchos) using 31P nuclear magnetic resonance spectroscopy
(NMR). Both 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)
and amiloride inhibited the development of the intracellular
alkalosis that normally develops in muscle during acute
hyperosmolality. Instead, exposure to hyperosmotic stress during ion
-exchange blockade resulted in a significant acidosis both
intracellularly and extracellularly. Arterial pH decreased 0.10+/
-0.04 pH units with sucrose infusion after either blocker, and
intracellular pH decreased 0.11+/-0.06 and 0.16+/-0.04 pH units upon
sucrose infusion after DIDS and amiloride, respectively. Ventilation
increased 79+/-28% and 122+/-100% during acute hyperosmolality after
ion-exchange blockade with either DIDS or amiloride. The results
suggest that intracellular pH may play a role in the ventilatory
response to acid-base perturbations. The data also indicate that both
Cl-/HCO3- and Na+/H+ exchange are involved in the development of the
intracellular alkalosis during hyperosmotically-induced extracellular
acidosis.
Received 14 December 1994; accepted in final form 30 October
1995.
APS Manuscript Number A1270-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95