FIG. 8.

Model to suggest how extreme astrocytic acidosis can be maintained for prolonged periods during hyperglycemic and complete ischemia. Previously, a model was proposed to explain how pH_o remained constant and astrocytic pH grew progressively more acidic during complete ischemia (Kraig et al., 1986). This model required that astrocytic membranes remain intact and that these cells progressively accumulate proton equivalents without absorbing bicarbonate buffer from the interstitial space. Acidic inhibition of membrane-based transport systems for proton equivalents was proposed as one means to retard egress of excess protons from cells. However, this phenomenon continued diffusion of nonionized lactic acid out of cells. The above schematic drawing deals with this latter issue. Astrocytic membranes are likely to remain permeable to nonionized organic acids (HA) such as lactic acid, so the concentration of HA can be expected to be equal within astrocytes and in extraglial space (EGS). If the astrocytic membrane is impermeable to charged species (H⁺ and A⁻), more acid will remain within astrocytes when more pH-related anions (such as lactate or bicarbonate) accumulate in the EGS. See text for further details.