• brain ischaemia;
  • lactic acidosis;
  • extracellular pH;
  • intracellular pH;
  • compartmentation of H +


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) -40 mm Hg] and hypercapnic (PaCO2 -80 mm Hg) animals. Irrespective of the preischaemic CO2 tension, δpHe was linearly related to tissue lactate content. Depending on the preischaemic glucose concentration, δpHe 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 (δ pHe-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 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.