Brain acidosis

Brain tissue acidosis is a result of either an increase in tissue PCO2 or an accumulation of acids produced by metabolism. Severe hypercapnia (arterial PCO2 around 300 mm Hg) may cause a fall in tissue pH to around 6.6 without any deterioration of the cerebral energy state or morphologic evidence of irreversible cell damage. In severe ischemia and tissue hypoxia, anaerobic glycolysis leads to lactic acid accumulation. This is aggravated by hyperglycemia and by a (trickling) residual blood flow. Under such circumstances lactate concentration in the tissue may increase to levels above 20 to 25 μmol/g (tissue wet weight), causing a decrease in pH to around 6.0. If lactic acidosis during ischemia or hypoxia reaches these excessive levels, metabolic and functional restitution is severely hampered upon subsequent recirculation and reoxygenation. In these circumstances cell morphology shows signs of irreversible damage. Conversely there is less damage if severe tissue lactic acidosis can be hindered. The deleterious effect of excessive lactic acidosis may be related to an influence on the following: synthesis and degradation of cellular constituents; mitochondrial function; cell volume control; postischemic blood flow; and stimulation of pathologic free radical reactions. Possibilities for therapeutic interventions include the avoidance of hyperglycemia, inhibition of glycolysis, and measures for increasing the buffer capacity of the brain. Brain tissue acidosis is a result of either an increase in tissue PCO2 or an accumulation of acids produced by metabolism. Severe hypercapnia (arterial PCO2 around 300 mm Hg) may cause a fall in tissue pH to around 6.6 without any deterioration of the cerebral energy state or morphologic evidence of irreversible cell damage. In severe ischemia and tissue hypoxia, anaerobic glycolysis leads to lactic acid accumulation. This is aggravated by hyperglycemia and by a (trickling) residual blood flow. Under such circumstances lactate concentration in the tissue may increase to levels above 20 to 25 μmol/g (tissue wet weight), causing a decrease in pH to around 6.0. If lactic acidosis during ischemia or hypoxia reaches these excessive levels, metabolic and functional restitution is severely hampered upon subsequent recirculation and reoxygenation. In these circumstances cell morphology shows signs of irreversible damage. Conversely there is less damage if severe tissue lactic acidosis can be hindered. The deleterious effect of excessive lactic acidosis may be related to an influence on the following: synthesis and degradation of cellular constituents; mitochondrial function; cell volume control; postischemic blood flow; and stimulation of pathologic free radical reactions. Possibilities for therapeutic interventions include the avoidance of hyperglycemia, inhibition of glycolysis, and measures for increasing the buffer capacity of the brain.