BRAIN ACIDOSIS INDUCED BY HYPERCARBIC VENTILATION ATTENUATES FOCAL ISCHEMIC-INJURY

Intracellular calcium toxicity appears to play a major role in cell de ath during cerebral ischemia. Such calcium enters the cell mainly thro ugh the N-methyl-D-aspartate subclass of the Postsynaptic glutamate re ceptor. Increased extracellular hydrogen ion concentration has been sh own recently to reduce N-methyl-D-aspartate-activated divalent cation currents. Therefore, we studied the effect of induced brain acidosis, via hypercarbic ventilation, as a potential therapeutic modality in fo cal cerebral ischemia. Brain acidosis reduced infarct volume in a biph asic manner, with maximal protection at approximately brain pH 6.8. Th e effect was lost at pH 6.5, presumably due to the effect of acidosis on glial glutamate uptake.