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The apparent first dissociation constant of carbonic acid has been defined in different ways in the literature. Harned and co-workers (8-10) have defined it in terms of molalities of the participating species, including H ions: Ks = mHmHCO3/mCO2. In contrast, Hastings and Sendroy have defined an apparent constant in which acidity is expressed as H ion activity: K'1 = aHmHCO3/mCO2. These constants differ by a factor gamma H, the activity coefficient of H ions at the prevailing ionic strength. Therefore, pK'1 is greater than pKs by an amount equal to -log gamma H, which, at mu = 0.16 M, is approximately 0.1. It is important that the correct value for the apparent dissociation constant or its logarithmic form be entered in the mass action expression or in the Henderson-Hasselbalch equation in order to prevent significant errors in the computation by means of these equations of quantities that cannot be directly measured. Specifically, for the derivation of bicarbonate concentration from PCO2 and pH (-log aH), pK'1 is to be used and not an uncorrected pKs.

Simultaneous measurements of tissue PCO2 (PtCO2), interstitial H+ concentration ([H+]o), and tissue lactate content were used to examine changes in interstitial HCO3- concentration ([HCO3-]o) during complete ischemia. In normoglycemic rats (blood glucose of 6-8 mM; neocortical ischemic-induced lactate content 8-12 mmol/kg) [H+]o increased from 7.22 +/- 0.02 to 6.79 +/- 0.02 pH (n = 3). By contrast, in hyperglycemic rats (blood glucose 18-75 mM; ischemic-induced lactate content 19-31 mmol/kg) [H+]o rose by a significantly larger amount to 6.19 +/- 0.02 pH (n = 7). Given that HCO3- is the predominant interstitial H+ buffer, changes in peak PtCO2 show why peak [H+]o were bimodally distributed compared with lactate content. Between 8 and 12 mmol/kg lactate, when peak PtCO2 rose from 99 to 186 Torr but [H+]o was constant at 6.79 pH, calculated [HCO3-]o increased from 11.9 to 21.9 mM. Then after transitional changes, peak PtCO2 and [H+]o remained constant at 389 +/- 9 Torr (n = 7) and 6.19 pH despite the fact that tissue lactate ranged from 19 to 31 mmol/kg lactate, respectively; [HCO3-]o must have remained constant at 12.3 +/- 0.7 mM (n = 7). Since ischemic brain continued to produce another 12 more mmol/kg of lactic acid above 19 mmol/kg lactate without further changes in PtCO2 or [H+]o, H+ and HCO3- must have been heterogeneously compartmented. The continued lactic acid production occurred in a compartment that occupied 36% of neocortical space. This compartment is likely to represent glial cells.