PT - JOURNAL ARTICLE AU - R P Simon AU - M Niro AU - R Gwinn TI - Brain acidosis induced by hypercarbic ventilation attenuates focal ischemic injury. DP - 1993 Dec 01 TA - Journal of Pharmacology and Experimental Therapeutics PG - 1428--1431 VI - 267 IP - 3 4099 - http://jpet.aspetjournals.org/content/267/3/1428.short 4100 - http://jpet.aspetjournals.org/content/267/3/1428.full SO - J Pharmacol Exp Ther1993 Dec 01; 267 AB - Intracellular calcium toxicity appears to play a major role in cell death during cerebral ischemia. Such calcium enters the cell mainly through the N-methyl-D-aspartate subclass of the postsynaptic glutamate receptor. Increased extracellular hydrogen ion concentration has been shown 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 focal cerebral ischemia. Brain acidosis reduced infarct volume in a biphasic manner, with maximal protection at approximately brain pH 6.8. The effect was lost at pH 6.5, presumably due to the effect of acidosis on glial glutamate uptake.