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Carbonic acid buffer changes during complete brain ischemia.

R P Kraig, W A Pulsinelli, F Plum

    The American Journal of Physiology
    |March 1, 1986
    PubMed
    Summary
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    During brain ischemia, interstitial bicarbonate levels adjust to buffer acidity. In hyperglycemic conditions, lactic acid production indicates compartmentalization within glial cells.

    Area of Science:

    • Neuroscience
    • Biochemistry
    • Physiology

    Background:

    • Brain ischemia leads to metabolic disturbances, including lactic acidosis.
    • Interstitial pH regulation is critical for neuronal function during ischemic events.
    • Bicarbonate (HCO3-) acts as a primary buffer for interstitial acidity (H+).

    Purpose of the Study:

    • To investigate the dynamics of interstitial bicarbonate concentration ([HCO3-]o) during complete brain ischemia.
    • To correlate changes in tissue PCO2 (PtCO2), interstitial [H+]o, and lactate content with [HCO3-]o.
    • To explore the compartmentalization of acid-base metabolism in the ischemic brain.

    Main Methods:

    • Simultaneous in vivo measurements of PtCO2, interstitial [H+]o, and tissue lactate.
    • Comparison between normoglycemic and hyperglycemic rat models during induced neocortical ischemia.

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  • Calculation of interstitial [HCO3-]o based on measured parameters and buffer principles.

    • Main Results:

    • Interstitial [H+]o increased significantly more in hyperglycemic rats (lactate 19-31 mmol/kg) compared to normoglycemic rats (lactate 8-12 mmol/kg).
    • Calculated interstitial [HCO3-]o increased with rising lactate in normoglycemic conditions but remained constant in hyperglycemic conditions despite further lactate accumulation.
    • Persistent lactic acid production in hyperglycemic ischemia occurred in a distinct compartment (36% of neocortical space), likely glial cells.

    Conclusions:

    • Interstitial bicarbonate concentration ([HCO3-]o) plays a crucial role in buffering acidity during ischemia, with its dynamics differing between normoglycemic and hyperglycemic states.
    • The data suggest heterogeneous compartmentalization of acid-base metabolism, particularly the production of lactic acid, within the ischemic brain.
    • Glial cells are implicated as a major site for continued lactic acid production during severe ischemia in hyperglycemic conditions.