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Related Experiment Videos

Hydrogen ion buffering during complete brain ischemia.

R P Kraig, W A Pulsinelli, F Plum

    Brain Research
    |September 9, 1985
    PubMed
    Summary
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    Brain interstitial [H+] changes during ischemia show a step-function relationship with tissue lactate, not a linear one. Astroglial ion transport likely explains this, preventing normal ion regulation and leading to brain infarction.

    Area of Science:

    • Neuroscience
    • Biochemistry
    • Physiology

    Background:

    • Ischemia leads to changes in brain interstitial [H+] (intracellular and extracellular hydrogen ion concentration).
    • Understanding the relationship between [H+]o and tissue lactate is crucial for quantifying these changes during ischemia.

    Purpose of the Study:

    • To quantify [H+] changes in the brain during ischemia.
    • To describe the relationship between interstitial [H+] ([H+]o) and peak tissue lactate after cardiac arrest.

    Main Methods:

    • Utilized H+-selective microelectrodes.
    • Employed enzyme fluorometric techniques.

    Main Results:

    • Observed a step-function relationship between [H+]o and tissue lactate, deviating from expected linear titration.

    Related Experiment Videos

  • Found that at higher blood glucose levels, brain lactate accumulated significantly, accompanied by a substantial rise in [H+]o.
  • Noted that [H+]o reached a steady-state, not equilibrium, with other brain compartments despite lactate accumulation.
  • Conclusions:

    • Astroglial ion-transport characteristics likely explain the observed [H+]o to tissue lactate relationship during ischemia.
    • Brain infarction may develop when brain cell plasma membranes lose their ion-transport regulatory capacity.