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Extra‐ and Intracellular pH in the Brain During Ischaemia, Related to Tissue Lactate Content in Normo‐and Hypercapnic rats
Author(s) -
Katsura Kenichiro,
Asplund Barbro,
Ekholm Anders,
Siesjö Bo K.
Publication year - 1992
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1992.tb00863.x
Subject(s) - chemistry , intracellular ph , intracellular , bicarbonate , medicine , brain tissue , endocrinology , ischemia , biochemistry , biology , organic chemistry
The objective of the present study was to assess the relationship between the amount of lactate accumulated during complete ischaemia and the ensuing changes in extra‐ and intracellular pH (pH e and pH i respectively). The preischaemic plasma glucose concentration of anaesthetized rats was varied by administration of glucose or insulin, pH e was determined in neocortex with ion‐sensitive microelectrodes, and tissue lactate and CO 2 contents were measured, tissue CO 2 tension being known from separate experiments. The experiments were carried out in both normocapnic [arterial CO 2 tension (PaCO 2 ) ‐40 mm Hg] and hypercapnic (PaCO 2 ‐80 mm Hg) animals. Irrespective of the preischaemic CO 2 tension, δpH e was linearly related to tissue lactate content. Depending on the preischaemic glucose concentration, δpH e varied from <0.4 to >1.4 units. The results thus fail to confirm previous results that the changes in pH e describe two plateau functions (δ pH e ‐0.5 and 1.1, respectively), with a transition zone at tissue lactate contents of 17–20 mmol kg −1 . Changes in pH; given in this study are based on the assumption of a uniform intracellular space. The pH, changed from a normal value of ‐7.0 to 6.5, 6.1 and 5.8 at tissue lactate contents of 10, 20 and 30 mmol kg‐ 1 . The intrinsic (non‐bicarbonate) buffer capacity, derived from these figures, was 23 mmol kg −1 pH −1 . Some differences in pH and in HCO 3 − concentration between extra‐ and intracellular fluids persisted in the ischaemic tissue. These differences were probably caused by a persisting membrane potential in the ischaemic cells.