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Eur J Neurosci. 1992;4(2):166-176. doi: 10.1111/j.1460-9568.1992.tb00863.x.

Extra- and Intracellular pH in the Brain During Ischaemia, Related to Tissue Lactate Content in Normo- and Hypercapnic rats.

The European journal of neuroscience

Kenichiro Katsura, Barbro Asplund, Anders Ekholm, Bo K. Siesjö

Affiliations

  1. Laboratory for Experimental Brain Research, Department of Neurobiology, Experimental Research Centre, Lund University Hospital, S-221 85 Lund, Sweden.

PMID: 12106379 DOI: 10.1111/j.1460-9568.1992.tb00863.x

Abstract

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 (pHe and pHi, respectively). The preischaemic plasma glucose concentration of anaesthetized rats was varied by administration of glucose or insulin, pHe was determined in neocortex with ion-sensitive microelectrodes, and tissue lactate and CO2 contents were measured, tissue CO2 tension being known from separate experiments. The experiments were carried out in both normocapnic [arterial CO2 tension (PaCO2) approximately 40 mm Hg] and hypercapnic (PaCO2 approximately 80 mm Hg) animals. Irrespective of the preischaemic CO2 tension, DeltapHe was linearly related to tissue lactate content. Depending on the preischaemic glucose concentration, DeltapHe varied from <0.4 to >1.4 units. The results thus fail to confirm previous results that the changes in pHe describe two plateau functions (DeltapHe approximately 0.5 and 1.1, respectively), with a transition zone at tissue lactate contents of 17 - 20 mmol kg-1. Changes in pHi given in this study are based on the assumption of a uniform intracellular space. The pHi changed from a normal value of approximately 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 HCO3- 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.

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