Carbonic acid buffer changes during complete brain ischemia

• Main Authors: KRAIG, RICHARD P., PULSINELLI, WILLIAM A., PLUM, FRED
• Format: Text
• Language: English
• Published: 1986
• Subjects: Article; Carbonic acid
• Online Access: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806331; http://www.ncbi.nlm.nih.gov/pubmed/3082219

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.